ORIGINAL_ARTICLE
Effect of Morphine Withdrawal Syndrome on Cerebral Ischemia Outcome in Rats
Objective(s)
Opioid abuse is still remained a major mental health problem, a criminal legal issue and may cause ischemic brain changes including stroke and brain edema. In the present study, we investigated whether spontaneously withdrawal syndrome might affect stroke outcomes.
Materials and Methods
Addiction was induced by progressive incremental doses of morphine over 7 days. Behavioral signs of withdrawal were observed 24, 48 and 72 hr after morphine deprivation and total withdrawal score was determined. Cerebral ischemia was induced 18-22 hr after the last morphine injection by placing a natural clot into the middle cerebral artery (MCA). Neurological deficits were evaluated at 2, 24 and 48 hr after ischemia induction, and infarct size and brain edema were determined at 48 hr after stroke.
Results
Morphine withdrawal animals showed a significant increase in total withdrawal score and decrease of weight gain during the 72 hr after the last morphine injection. Compared to the addicted and control animals, infarct volume and brain edema were significantly increased in the morphine deprived animals (P< 0.05) at 48 hr after cerebral ischemia. Also, neurological deficits were higher in the morphine-withdrawn rats at 48 hr after stroke (P< 0.05).
Conclusion
Our data indicates that spontaneous withdrawal syndrome may worsen stroke outcomes. Further investigations are necessary to elucidate mechanisms of opiate withdrawal syndrome on stroke.
https://ijbms.mums.ac.ir/article_4945_5af6302caa4413c66fc710ad72e8414b.pdf
2011-01-01
1
8
10.22038/ijbms.2011.4945
Addiction
Cerebral ischemia
Embolic stroke
Morphine withdrawal syndrome
Opiates
Mohammad
Allahtavakoli
m_alahtavakoli@rums.ac.ir
1
Department of Physiology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
LEAD_AUTHOR
Ruhollah
Moloudi
2
Department of Physiology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
AUTHOR
Mohammad Ebrahim
Rezvani
3
Department of Physiology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
AUTHOR
Ali
Shamsizadeh
alishamsy@gmail.com
4
Department of Physiology, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran
AUTHOR
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12. Feng P, Meissler JR, Adler MW,Eisenstein TK. Morphine withdrawal sensitizes mice to lipopolysaccharide: elevated TNF-alpha and nitric oxide with decreased IL-12. J Neuroimmunol 2005; 164:57-65.
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17. Allahtavakoli M, Moloudi R, Arababadi MK, Shamsizadeh A, Javanmardi K. Delayed post ischemic treatment with rosiglitazone attenuates infarct volume, neurological deficits and neutrophilia after embolic stroke in rat. Brain Res 2009; 19:121-127.
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24. Giuliani D, Leone S, Mioni C, Bazzani C, Zaffe D, Botticelli AR, et al. Broad therapeutic treatment window of (Nle(4), D-Phe(7))alpha-melanocyte-stimulating hormone for long-lasting protection against ischemic stroke, in Mongolian gerbils. Eur J Pharmacol 2006; 538:48-56.
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25. Kao TK, Ou YC, Liao SL, Chen WY, Wang CC, Chen SY, et al. Opioids modulate post-ischemic progression in a rat model of stroke. Neurochem Int 2008; 52:1256-1265.
25
ORIGINAL_ARTICLE
The Laxative and Prokinetic Effects of Rosa damascena Mill in Rats
Objective(s) This study was aimed to assess the possible laxative and prokinetic effects of the boiled extract of Rosa damascena. Materials and Methods Rats in two groups (n= 7) of test and control were gavaged either with the extract or placebo, respectively. The number, weight and water percentage of feces were studied up to 24 hr. In order to assess the possible osmotic laxative effects of the drug, the jejunum in anesthetized rats (n= 7) was randomly divided into 4 cm segments and 0.5 ml of the extract, lactulose or saline was injected in each segment. The volumes of the contents in each segment were measured after 1 hr. In order to assess the intestinal transit time, fasting rats were gavaged with either the extract or placebo. Thirty minutes following the last medication, all rats were gavaged with phenol red and methyl cellulose (1.5 ml). The test and the control rats, in groups of 4, were sacrificed at 30 min, 1, 2 and 4 hr, and the amounts of the phenol red in various parts of the gastrointestinal tract were measured. Results Boiled extract of R. damascena significantly increased feces number and its percentage of water, but had no effects on the transit time of intestinal ingesta. The volume of the contents in jejunum segments had significantly increased with the extract or lactulose compared to placebo. Conclusion Boiled extract of R. damascena apparently exerts its laxative effects, at least in part, via osmotic infiltration of fluids into the intestine.
https://ijbms.mums.ac.ir/article_4948_22215c29ff45c20957241aba0cc9d3a1.pdf
2011-01-01
9
16
10.22038/ijbms.2011.4948
Laxative
Prokinetic
Rosa damascena
Reza
Arezoomandan
1
Department of Physiology, School of Basic Sciences, Ferdowsi University of Mashhad, Iran
AUTHOR
Hamid Reza
Kazerani
kazrani@yahoo.co.uk
2
Department of Physiology, Faculty of Veterinary Medicine, Ferdowsi University of Mashhad, Iran
LEAD_AUTHOR
Morteza
Behnam-Rasooli
3
Department of Physiology, School of Basic Sciences, Ferdowsi University of Mashhad, Iran
AUTHOR
1. Kovats E. Composition of essential oils. Part 7. Bulgarian oil of rose (Rosa damascena Mill.). J Chromatogr 1987; 406:185-222.
1
2. Wood G, Bache F. The dispensatory of the United States of America. 4th ed. USA: Griggand Elliot; 1839.
2
3. AveSina AA. Law in medicine. (Translated by: Sharafkhandy A), Iran:Ministry of Guidance Publication; 1990. p. 129–131.
3
4. Zargari A. Medicinal plants. 5th ed. Iran: Tehran University Press; 1992. p. 281-284.
4
5. Ulusoy S, Boşgelmez-Tinaz G, Seçilmiş-Canbay H. Tocopherol, carotene, phenolic contents and antibacterial properties of rose essential oil, hydrosol and absolute. Curr Microbiol 2009; 59:554-558.
5
6. Ozkan G, Sagdic O, Baydar NG, Baydar H. Antioxidant and antibacterial activities of Rosa damascena flower extracts. Food Sci Technol Int? 2004; 10:277-281.
6
7. Basim E, Basim H. Antibacterial activity of Rosa damascena essential oil. Fitoterapia 2003; 74:394-396.
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8. Achuthan CR, Babu BH, Padikkala J. Antioxidant and hepatoprotective effects of Rosa damascena. Pharm Biol 2003; 41:357-361.
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9. Mahmood N, Piacente S, Pizza C, Burke A, Khan AI, Hay AJ. The anti-HIV activity and mechanisms of action of pure compounds isolated from Rosa damascena. Biochem Biophys Res Commun 1996; 229:73-79.
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10. Shafei MN, Rakhshandah H, Boskabady MH. Antitussive Effect of Rosa damascena in Guinea pigs. Iran J Pharm Res 2003; 2:231-234.
10
11. Kovats E. Composition of essential oils. Part 7. Bulgarian oil of rose (Rosa damascena Mill.). J Chromatogr 1987; 406:185-222.
11
12. Wood G, Bache F. The dispensatory of the United States of America. 4th ed. USA: Griggand Elliot; 1839.
12
13. AveSina AA. Law in medicine. (Translated by: Sharafkhandy A), Iran:Ministry of Guidance Publication;
13
1990. p. 129–131.
14
14. Zargari A. Medicinal plants. 5th ed. Iran: Tehran University Press; 1992. p. 281-284.
15
15. Ulusoy S, Boşgelmez-Tinaz G, Seçilmiş-Canbay H. Tocopherol, carotene, phenolic contents and antibacterial properties of rose essential oil, hydrosol and absolute. Curr Microbiol 2009; 59:554-558.
16
16. Ozkan G, Sagdic O, Baydar NG, Baydar H. Antioxidant and antibacterial activities of Rosa damascena flower extracts. Food Sci Technol Int? 2004; 10:277-281.
17
17. Basim E, Basim H. Antibacterial activity of Rosa damascena essential oil. Fitoterapia 2003; 74:394-396.
18
18. Achuthan CR, Babu BH, Padikkala J. Antioxidant and hepatoprotective effects of Rosa damascena. Pharm Biol 2003; 41:357-361.
19
19. Mahmood N, Piacente S, Pizza C, Burke A, Khan AI, Hay AJ. The anti-HIV activity and mechanisms of
20
action of pure compounds isolated from Rosa damascena. Biochem Biophys Res Commun 1996; 229:73-79.
21
20. Shafei MN, Rakhshandah H, Boskabady MH. Antitussive Effect of Rosa damascena in Guinea pigs. Iran J Pharm Res 2003; 2:231-234.
22
21. Kimura T, Iwasaki N, Yokoe JI, Haruta S, Yokoo Y, Ogawara KI, et al. Analysis and prediction of absorption profile including hepatic first-pass metabolism of n-methyltyramine, a potent stimulant of gastrin release present in beer, after oral ingestion in rats by gastrointestinal-transit-absorption model. Drug Metab Dispos 2000; 28:577-81.
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22. Harris LA. Current mechanisms of action in treatment of chronic constipation and irritable bowel syndrome. Adv Stud Med 2006; 6:S237-S242.
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32
ORIGINAL_ARTICLE
Evaluation of Porin Interaction with Adenine Nucleotide Translocase and Cyclophilin-D Proteins after Brain Ischemia and Reperfusion
Objective (s) Porin is a mitochondrial outer membrane channel, which usually functions as the pathway for the movement of various substances in and out of the mitochondria and is considered to be a component of the permeability transition (PT) pore complex that plays a role in the PT. We addressed the hypothesis that porin interacts with other mitochondrial proteins after ischemic injury. Materials and Methods For this purpose, we used in vivo 4-vessel occlusion model of rat brain and porin purification method by hydroxyapatite column. After SDS gel electrophoresis and silver nitrate staining, Western blotting was done for porin, adenine nucleotide translocase and cyclophilin-D proteins. Results Porin was purified from mitochondrial mixture in ischemic brain and control groups. Investigation of interaction of adenine nucleotide transposes (ANT) and cyclophilin-D with porin by Western blotting showed no proteins co-purified with porin from injured tissues. Conclusion The present study implies that there may not be interaction between porin, and ANT or cyclophilin-D, and if there is any, it is not maintained during the purification procedure.
https://ijbms.mums.ac.ir/article_4951_9f9c69a1010a2eb6d67066b4c2d0bb0a.pdf
2011-01-01
17
24
10.22038/ijbms.2011.4951
Ischemia
Mitochondrial permeability transition pore
Porins
Reperfusion
Mohammad Ali
Atlasi
atlasima@gmail.com
1
Anatomical Sciences Research Center, Kashan University of Medical Sciences, Kashan, Iran
LEAD_AUTHOR
Jose Luis
Perez Velazquez
2
Department of Neurology and Pediatrics, the Hospital for Sick Children, Brain and Behavior Programme, University of Toronto, Ontario, Canada
AUTHOR
1. Halestrap AP, Clarke SJ, Javadov SA. Mitochondrial permeability transition pore opening during myocardial reperfusion-a target for cardio protection. Cardiovasc Res 2004; 61:372-385.
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2. Halestrap AP. Calcium, mitochondria and reperfusion injury: a pore way to die. Biochem Soc Trans 2006; 34:232–237.
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3. Du C, Fang M, Li Y, Li L, Wang X. Smac, a mitochondrial protein that promotes cytochrome cdependent caspase activation by eliminating IAP inhibition. Cell 2000; 102:33-42.
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5. Tsujimoto Y, Shimizu S. Bcl-2 family: life-or-death switch. FEBS Lett 2000; 466:6–10.
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6. Leung AW, Halestrap AP. Recent progress in elucidating the molecular mechanism of the mitochondrial permeability transition pore. Biochim Biophys Acta 2008; 1777:946–952.
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7. Zoratti M, Szabo I.The mitochondrial permeability transition. Biochim Biophys Acta 1995; 1241:139–176.
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8. Bernardi P.Mitochondrial transport of cations: channels, exchangers, and permeability transition. Physiol Rev 1999; 79:1127–1155.
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9. Crompton M. The mitochondrial permeability transition pore and its role in cell death. Biochem J 1999; 341:233–249.
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10. Bernardi P,Petronilli V,Di Lisa F, Forte M. A mitochondrial perspective on cell death. Trends Biochem Sci 2001; 26:112–117.
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11. Zamzami N, Kroemer G. The mitochondrion in apoptosis: how Pandora's box opens. Nat. Rev. Mol. Cell. Biol. 2001; 2: 67–71
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12. Halestrap AP. Calcium-dependent opening of a non-specific pore in the mitochondrial inner membrane is inhibited at pH values below 7-implications for the protective effect of low pH against chemical and hypoxic cell damage. Biochem J 1991; 278:715-719.
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13. Nicolli A, Basso E, Petronilli V, Wenger RM, Bernardi P. Interactions of cyclophilin with the mitochondrial inner membrane and regulation of the permeability transition pore, a cyclosporin a-sensitive channel. J Biol Chem 1996; 271:2185-2192.
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14. Cesura AM, Pinard E, Schubenel R, Goetschy V, Friedlein A, Langen H, et al. The voltage-dependent anion channel is the target for a new class of inhibitors of the mitochondrial permeability transition pore. J Biol Chem 2003; 278:49812–49818.
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15. Perez Velazquez JL, Frantseva MV, Huzar DV, Carlen PL. Mitochondrial porin required for ischemia-induced mitochondrial dysfunction and neuronal damage. Neuroscience 2000; 97:363-369.
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16. Pagnussat AS, Faccioni-Heuser MC, Netto CA, Achaval M. An ultrastructural study of cell death in the CA1 pyramidal field of the hippocampus in rats submitted to transient global ischemia followed by reperfusion. J Anat 2007; 211:589-599.
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18. Vieira HL, Haouzi D, El Hamel C, Jacotot E, Belzacq AS, Brenner C, et al. Permeabilization of the mitochondrial inner membrane during apoptosis: impact of the adenine nucleotide translocator. Cell Death Differ 2000; 7:1146-1154.
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19. Machida K, Osada H. Molecular interaction between cyclophilin-D and adenine nucleotide translocase in cytochrome c release: does it determine whether cytochrome release is dependent on permeability transition or not? Ann N Y Acad Sci 2003; 1010:182-185.
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20. Crompton M, Virji S, Ward JM. Cyclophilin-D binds strongly to complexes of the voltage-dependent anion channel and the adenine nucleotide translocase to form the permeability transition pore. Eur J Biochem 1998; 258:729-735.
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21. Woodfleld K, Ruck A, Brdiczka D, Halestrap AP. Direct demonstration of a specific interaction between cyclophilin-D and the adenine nucleotide translocase confirms their role in the mitochondrial permeability transition. Biochem J 1998; 336:287-290.
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22. Li Y, Johnson N, Capano M, Edwards M, Crompton M. Cyclophilin-D promotes the mitochondrial permeability transition but has opposite effects on apoptosis and necrosis. Biochem J 2004; 383:101–109.
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23. Kroemer G, Galluzzi L, Brenner C. Mitochondrial permeabilization in cell death. Physiol Rev 2007; 87: 99–163.
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24. Lisa Di, Canton M, Menabò R, Kaludercic N, Bernardi P. Mitochondria and cardioprotection, Heart Fail Rev 2007; 12:249–260.
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25. Baines CP, Kaiser RA, Sheiko T, Craigen WJ, Molkentin JD.Voltage-dependent anion channels are dispensable for mitochondrial-dependent cell death. Nat Cell Biol 2007; 9:550–555.
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26. Kokoszka JE, Waymire KG, Levy SE, Sligh JE, Cai J, Jones DP, et al. The ADP/ATP translocator is not essential for the mitochondrial permeability transition pore. Nature 2004; 427:461-465.
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27. Pulsinelli WA, Brierley JB. A new model of bilateral hemispheric ischemia in the unanesthetized rat. Stroke 1979; 10:267-272.
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28. De Pinto V, Prezioso G, Palmieri F. A simple and rapid method for purification of the mitochondrial porin from mammalian tissues. Biochim Biophys Acta 1987; 905:499-502.
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29. Perez Velazquez JL, Kokarovtseva L, Weisspapir M, Frantseva MV. Anti-porin antibodies prevent excitotoxic and ischemic damage to brain tissue. J Neurotrauma 2003; 20:633-647.
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30. De Pinto V, Benz R, Palmieri F. Interaction of non-classical detergents with the mitochondrial porin. A new purification procedure and characterization of the pore- forming unit. Eur. J Biochem 1989; 183:179 –187.
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31. Shimizu S, Matsuoka Y, Shinohara Y, Yoneda Y, Tsujimoto Y. Essential role of voltage-dependent anion channel in various forms of apoptosis in mammalian cells. J Cell Biol 2001; 152:237–250.
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32. Fagian MM, Pereira-da-Silva L, Martins IS, Vercesi AE.Membrane protein thiol cross-linking associated with the permeabilization of the inner mitochondrial membrane by Ca2+ plus Prooxidants. J Biolo Chem 1990; 265:19955-19960.
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33. Halestrap AP, McStay GP, Clarke SJ. The permeability transition pore complex: another view. Biochimie 2002; 84:153-166.
33
34. Brustovetsky N, Tropschug M, Heimpel S, Heidkaemper D, Klingenberg, M. A large Ca2+-dependent channel formed by recombinant ADP/ATP carrier from Neurospora crassa resembles the mitochondrial permeability transition pore. Biochemistry 2002; 41:11804–11811.
34
35. Baines CP.The mitochondrial permeability transition pore and ischemia reperfusion injury. Basic Res Cradiol 2009; 104:181-188.
35
36. Halestrap AP. What is the mitochondrial permeability transition pore? J Mol Cell Cardiol 2009; 46:821–831.
36
37. Kim J-S, He L, Lemasters JJ. Mitochondrial permeability transition: a common pathway to necrosis and apoptosis. Biochem Biophys Res Commun 2003; 304:463-470.
37
38. Krauskopf A, Eriksson O, Craigen WJ, Forte MA, Bernardi P. Properties of the permeability transition in VDAC1-/- mitochondria. Biochim Biophys Acta 2006; 1757:590–595.
38
ORIGINAL_ARTICLE
Mesenchymal Stem Cells Derived from Rat Epicardial Versus Epididymal Adipose Tissue
Objective(s) Some investigation has indicated that adipose-derived stem cells possess different surface epitopes and differentiation potential according to the localization of fat pad from which the cells were derived. In the present study proliferation capacity and aging of such cells were explored. Materials and Methods Adherent cells were isolated from the collagenase digests of adipose tissues excised from rat epicardial and epididymal regions and propagated with several subcultures. The cells were then investigated whether or not they were able to differentiate into bone, cartilage and adipose cell lineages. Studied cells from two adipose tissues were also compared with respect to their in vitro proliferation capacity. The presence of senescent cells in the culture was determined and compared using senescence-associated (SA) ß-galactosidase staining method. Results Successful differentiations of the cells were indicative of their mesenchymal stem cells (MSCs) identity. Epicardial adipose-derived cells tended to have a short population doubling time (45±9.6 hr) than the epididymal adipose-derived stem cells (69±16 hr, P< 0.05). Colonogenic activity and the growth curve characteristics were all better in the culture of stem cells derived from epicardial compared to epididymal adipose tissue. Comparatively more percentage of senescent cells was present at the cultures derived from epididymal adipose tissue (P< 0.05). Conclusion Our data emphasize on the differences existed between the stem cells derived from adipose depots of different anatomical sites in terms of their proliferative capacity and in vitro aging. Such data can help understand varying results reported by different laboratories involved in adipose stem cell investigations.
https://ijbms.mums.ac.ir/article_4952_d9b84fd2b689c2468382b1d4ad329c4c.pdf
2011-01-01
25
34
10.22038/ijbms.2011.4952
Adipose tissue
Cell aging
Cell differentiation
Cell Proliferation
Mesenchymal stem cell
Mohamadreza
Baghaban Eslaminejad
eslami@royaninstitute.org
1
Department of Stem Cell and Developmental Biology, Royan Institute for Stem Cell Biology and Technology, Iranian Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
LEAD_AUTHOR
Soura
Mardpour
2
Department of Developmental Biology, University of Science and Culture, Tehran, Iran
AUTHOR
Marzieh
Ebrahimi
3
Department of Stem Cell and Developmental Biology, Royan Institute for Stem Cell Biology and Technology, Iranian Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
AUTHOR
1. Friedenstein AJ, Piatetzky II, Petrakova KV. Osteogenesis in transplants of bone marrow cells. J Embryol Exp Morphol 1966; 16:381-390.
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2. Friedenstein J, Chailakhjan RK, Lalykina KS. The development of fibroblast colonies in monolayer cultures of guinea-pig bone marrow and spleen cells. Cell Tissue Kinet 1970; 3: 393-403.
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3. Baksh D, Song L, Tuan RS. Adult mesenchymal stem cells: Characterization, differentiation and application in cell therapy. Mol Med 2004; 8:301-136.
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4. Jankowsk RJ, Deasy BM, Huard J. Muscle-derived stem cells. Gene Ther 2002; 9:642-647.
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5. Miura M, Grothos S, Zhao M, Lu B, Fisher LW, Robery PG, et al. Stem cells from human exfoliated decidusus teeth. Proceed. Nation Acad Sci USA 2003; 100:5807-5812.
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6. Zvaifler NJ, Marinova-Mutafchieva L, Adams G, Edwards CJ, Moss J, Burger JA, et al. Mesenchyamal precursor cells in the blood of normal individuals. Arthritis Res 2000; 2:477-488.
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7. Erices A, Conget P, Miguell JJ. Mesenchymal progenitor cells in human umbilical cord blood. Br J Haematol 2000; 109:235-242.
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8. Eslaminejad MB, Taghiyar L. Mesenchymal stem cell purification from the articular cartilage cell culture. Iran J Basic Med Sci 2008; 3:146-153.
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9. Wickham MQ, Erickson GR, Gimble JM, Vail TP, Guilak F. Multipotent stromal cells derived from infrapatellar fat pad of knee. Clin Orthop 2003; 412:196-212.
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10. Rodbell M. Metabolism of isolated fat cells. II. The similar effects of phospholipase C (Clostridium perfringensm alpha toxin) and of insulin on glucose and amino acid metabolism. J Biol Chem 1966; 241:130-139.
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12. Lalikos JF, Li YQ, Roth TP, Doyle JW, Matory WE, Lawrence WT. Biochemical assessment of cellular damage after adipocyte harvest. J Surg Res 1997; 70:95-100.
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13. Hattori H, Sato M, Masuoka K, Ishihara M, Kikuchi T, Matsui T, et al. Osteogenic potential of human adipose tissue-derived stromal cells as an alternative stem cell source. Cells Tissues Organs 2004; 178:2 12.
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14. Guilak F, Awad HA, Fermor B, Leddy HA, Gimble JM. Adipose-derived adult stem cells for cartilage tissue engineering. Biorheology 2004; 41:389-399.
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15. Planat-Benard V, Silvestre JS, Cousin B, André M, Nibbelink M, Tamarat R, et al. Plasticity of human adipose lineage cells toward endothelial cells: physiological and therapeutic perspectives. Circulation 2004; 109:656-663.
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statement. Cytotherapy 2006; 4:315-317.
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34
ORIGINAL_ARTICLE
Lectin Histochemical Study of Vasculogenesis During Rat Pituitary Morphogenesis
Objective(s)
The aim of this study was to investigate glycoconjugates distribution patterns as well as their changes during the course of pituitary portal vasculogenesis and angiogenesis.
Materials and Methods
Formalin fixed paraffin sections of 10 to 20 days of Sprague Dawly rat fetuses were processed for histochemical studies using four different horseradish peroxidase (HRP) conjugated lectins. Orange peel fungus (OFA), Vicica villosa (VVA), Glycine max (SBA) and Wistaria floribunda (WFA) specific for α-L Fucose, D-Gal, α, ß-D-GalNAc and D- GalNAc terminal sugars of glycoconjugates respectively.
Results
Our finding indicated that adenohypophysal cells reacted with OFA on gestational day 10 (E10) and increased progressively to E14. Staining intensity did not change from days 14 to17, then after increased following days to E20 significantly (P< 0.05). A few cells around Rathke’s pouch reacted with VVA on E13, increased to E14 and decreased significantly afterward (P< 0.05). Reaction of some cells around Rathke’s pouch reacted with SBA on E14. This visible reaction was the same as E18 and decreased later (P< 0.05). Many cells around Rathke’s pouch reacted with WFA on E13 and increased on E 14 and E15 and decreased thereafter (P< 0.05).
Conclusion
Reactions of OFA and other tested lectins with endothelial cells around Rathke’s pouch and developing pars distalis were different. These results suggest that embryonic origin of hypophiseal pituitary portal (HPP) system endothelial cells are not the same and our finding also indicated that glycoconjugates with terminal sugars α-L-Fucose, D-Gal, α, ß-D-GalNAc may play critical role(s) in cell interactions and tissue differentiations such as vasculogensis and angiogenesis as well as other developmental precursors in formation of the pituitary gland.
https://ijbms.mums.ac.ir/article_4953_53e70f742672227f6a4b6a85391f2ce2.pdf
2011-01-01
35
41
10.22038/ijbms.2011.4953
Angiogenesis
Glycoconjugates
Lectin
Pituitary
Rat
Ali Reza
Ebrahimzadeh Bideskan
ebrahimzadehba@mums.ac.ir
1
Department of Anatomy, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Mohammad Mehdi
Hassanzadeh Taheri
2
Department of Anatomy, School of Medicine, Birjand University of Medical Sciences, Birjand, Iran
AUTHOR
Mohammad Reza
Nikravesh
nikraveshmr@mums.ac.ir
3
Department of Anatomy, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Ali Reza
Fazel
4
Department of Anatomy, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
1. Stepien HM, Kolomecki K, Pasieka Z, Komorowski J, Stepien T, Kuzdak K. Angiogenesis of endocrine gland tumors new molecular targets in diagnostics and therapy. Eur J Endocrinol 2002; 146:143-151.
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2. Jessica DG,William G. Angiogenesis. Med Rev 2002; 3:38-143.
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3. Hirashima M. Regulation of endothelial cell differentiation and arterial specification by VEGF and Notch signaling. Anat Sci Int 2009 84:95-101.
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4. Goldie LC, Nix MK, Hirschi KK. Embryonic Vasculogenesis and hematopoietic specification. Organogenesis 2008; 4:257-63.
4
5. Domenico R, Angelo V, Macro P.The discovery of angiogenic factors: A historical review. Gen Pharmacol 2002; 23:227-231.
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6. Miosge N, Gotz W, Quondamatteo F, Herken R. Comparison of lectin binding patterns in malformation and normal human embryos and fetus. Teratology 1998; 57:85-92.
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7. Pratima NM, Avraham S. Carbohydrate-recognition and angiogenesis. Cancer Metastasis Rev 2000; 19:51-57.
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8. Dubois PM, Elamraoui A. Embryology of the pituitary gland.Trends Endocrinol Metab 1995; 6:1-7.
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9. Szabo K, Csanyi K. The blood supply of the developing hypophysis in rat embryos. Verh Anat Ges 1981; 75:507-509.
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12. Shahal M, Thoma J, Shelley NM, Anne E. Selective binding of lectins to embryonic chicken Vasculature. J Histochem Cytochem 2003; 51:597-604.
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15. Budihardjo H, Welim MT, Rainer H. Appearance of lectin-binding sites during vascularization of the primordium of the central nervous system in 10 to 12-day-old mouse embryos. Cell Tissue Res 1989; 255:1-5.
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16. Helimut G, Konrad B, Telemenakis I, Modlich U, Walther K. Ovarian angiogenesis phenotypic characterization of endothelial cells in a physiological model of blood vessel growth and regression. Am J Pathol 19995; 147:339-351.
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19. Fazel AR, Schulte BA, Spicer SS. Glycoconjugate unique to migrating primordial germ cell differs with Genera. Anat Rec 1990: 228:177-184.
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20. Hassanzadeh Taheri MM, Nikravesh MR, D Jalali M, Fazel AR, Ebrahimzadeh AR. Distribution of specific glycoconjugates in early mouse embryonic notochord and paraxial mesenchyme. Iran Biomed J 2005; 9:21-26.
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21. Ahi M, Zamansoltani F, Hassanzadeh Taheri MM, Ebrahimzadeh Bideskan AR. The role of GalNac terminal sugar on adernal gland development. Adv Biol Res 2007; 1:34-36.
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22. Sheng HZ, Westphal H. Early steps in pituitary organogenesis. Trends Genet 1999; 15:238-240.
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23. Micha W, Frontczak B. New vessel formation after surgical brain injury in the rat’s cerebral cortex II. Formation of the blood vessels distal to the surgical injury. Acta Neurobiol Exp 2003; 63: 77-82.
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24. Szabo K, Csanyi K. The vascular architecture of the developing pituitary-median eminence complex in Rat. Cell Tissue Res 1982; 224:563-577.
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25. Szabo K. Origin of the adenohypophiseal vessels in the Rat. J Anat 1987; 154: 229-235.
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26. Risau W, Flamme I.Vasculogenesis. Annu Rev Cell Dev Biol 1995; 11:73-91.
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28. Jakobsson L, Domogatskaya A, Tryggvason K, Edgar D, Claesson-Welsh L. Laminin deposition is dispensable for vasculogenesis but regulates blood vessel diameter independent of flow. FASEB J 2008; 22:1530-1539.
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30
ORIGINAL_ARTICLE
The Effect of Chronic Administration of Aegle Marmelos Seed Extract on Learning and Memory in Diabetic Rats
Objective(s)
Diabetes mellitus is associated with disturbances of learning and memory and cognitive functioning. Aegle marmelos Corr. from Rutaceae family is widely used in Iranian folk medicine for the treatment of diabetes mellitus. Considering the beneficial antidiabetic and antioxidant potential of A. marmelos, this study was conducted to evaluate the effect of oral administration of A. marmelos on learning and spatial memory in diabetic rats using Morris water maze test.
Materials and Methods
Considering the beneficial antidiabetic potential of A. marmelos, this study was conducted to evaluate the effect of chronic oral administration of A. marmelos as cognitive enhancer, on learning and spatial memory in diabetic rats using Morris water maze test. Male Wistar rats were randomly divided into normal-control, diabetic-control, and A. marmelos-treated diabetic groups (100, 250 and 500 mg/kg, p.o.). Animals were treated for 4 weeks by A. marmelos or normal saline. Diabetes was induced by a single dose i.p. injection of streptozotocin (45 mg/kg). In each group of animals, spatial learning and memory parameters were analyzed.
Results
Clear impairment of spatial learning and memory was observed in diabetic group versus normal-control group. A. marmelos showed dose dependent improvement in spatial learning and memory parameters that swimming time (Escape Latency) in normal-control and A. marmelos-treated diabetic animals rats was significantly (P< 0.01) lower than diabetic-control, while swimming speed was significantly (P< 0.05) higher.
Conclusion
The study demonstrated that A. marmelos has significant protective affect against diabetes-induced spatial learning and memory deficits. This effect could be attributed to hypoglycemic, hypolipidemic and antioxidant activity of A. marmelos.
https://ijbms.mums.ac.ir/article_4954_de999b2cd7bb3b5794a669289010fbca.pdf
2011-01-01
42
48
10.22038/ijbms.2011.4954
Aegle marmelos
Diabetes
Morris Water Maze
Spatial learning and Memory
Amir
Farshchi
farshchi_a@razi.tums.ac.ir
1
School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
LEAD_AUTHOR
Golbarg
Ghiasi
2
School of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Samireh
Farshchi
3
Department of otolaryngology, Amiralam Hospital, Tehran University of Medical Sciences, Tehran, Iran.
AUTHOR
Amin
Taleb Ghobadi
4
School of Medicine, Lorestan University of Medical Sciences, Khoramabad, Iran
AUTHOR
1. Biessels GJ, Kappelle AC, Bravenboer B, Erkelens DW, Gispen WH. Cerebral function in diabetes mellitus. 1994; 37:643–650.
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2. Vinik AI, Holland MT, Le Beau JM, Liuzzi FJ, Stansberry KB, Colen LB. Diabetic neuropathies. Diabetes Care 1992; 15:1926–1975.
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4. Ryan CM.Neurobehavioral complications of type I diabetes. Examination of possible risk factors. Diabetes Care 1988; 11:86–93.
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5. Tun PA, Nathan DM, Perlmuter LC. Cognitive and affective disorders in elderly diabetics. Clin Geriatr Med 1990; 6:731–746.
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6. Nandkarni AK. Indian Materia Medica. 3rd ed.Bombay: Popular Prakshan; 1976.
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7. Kirtikar KR, Basu BD. Indian Medicinal Plant. Calcutta: Lalit Mohan Publication; 1935.
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9. Ave-Sina A. Law in Medicine. Tehran: Soroosh Press; 1988.
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10. Alam MM, Siddiqui MB, Husain W. Treatment of diabetes through herbal drug in rural India. Fitoterapia 1990; 61:240–242.
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11. Prakash V. Diabetes management-Some useful herbs. Shishir: Jeevaniya;1992.Vol.4.
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12. Chakrabarti B. Mallick C, Battacharya S. Studies on the green leaves of Aegle marmelos and Piper nigrum on the glucose and cholesterol levels of blood in diabetes mellitus. Indian Med Forsch 1960; 9:285–286.
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13. Karunanyake EH, Welhinda J, Sirimanne SR, Sinnadorai G. Oral hypoglycemic activity in some medicinal plants from Sri Lanka. J Ethnopharmacol 1984; 11:223–231.
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14. Kamalakkannan N, Prince PSM. Hypoglycemic effect of water extract of Aegle marmelos fruits in sreptozotocin diabetic rats. J Ethnopharmacol 2003; 87:207–210.
14
15. Kamalakkannan N, Prince PSM. Antidiabetic and antioxidant activity of Aegle marmelos extract in streptozotocin induced diabetic rats. Pharm Biol 2004; 42:125–130.
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16. Ponnachan PTC, Paulose CS, Panikkar KR. Hypoglycemic effect of alkaloid preparation from leaves of Aegle marmelos. Amala Res Bull 1993; 13:37–41.
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17. Ponnachan PTC, Paulose CS, Panikkar KR. Effect of leaf extract of Aegle marmelos in diabetic rats. Indian J Exp Biolo 1993; 31:345–347.
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18. Seema PV, Sudha B, Padayatti PS, Abraham A, Raghu KG, Paulose CS. Kinetic studies of purified malate dehydrogen-ase in liver of streptozotocin-diabetic rats and the effect of leaf extract of Aegle marmelose (L) Correa ex Roxb. Indian J Exp Biolo 1996; 34:600–602.
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19. Das AV, Padayatti PS, Paulose CS. Effect of leaf extract of Aegle marmelose (L) Correa ex Roxb. On histological and ultrastructural changes in tissues of streptozotocin induced diabetic rats. Indian J Exp Biolo 1996; 34:341–345.
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22. Kesari AN, Gupta RK, Singh SK, Diwakar S, Watal G. Hypoglycemic and antihyperglycemic activity of Aegle marmelos seed extract in normal and diabetic rats. J Ethnopharmacol 2006; 107: 374–379.
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23. Sabu MC, Kuttan R. Antidiabetic activity of Aegle marmelos and its relationship with its antioxidant properties. Indian J Physiol Pharmacol 2004; 48:81-88.
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24. Upadhya S, Shanbhag KK, Suneetha G, Balachandra Naidu M, Upadhya S.A study of hypoglycemic and antioxidant activity of Aegle marmelos in alloxan induced diabetic rats. Indian J Physiol Pharmacol 2004; 48:476-480.
24
25. Kamalakkannan N, Stanely Mainzen Prince P. Effect of Aegle marmelos Correa. (Bael) fruit extract on tissue antioxidants in streptozotocin diabetic rats. Indian J Exp Biol 2003; 41:1285-1288.
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26. Brosky G, Logothelopoulos J. Streptozotocin diabetes in the mouse and guinea pig. Diabetes 1969; 18:606–609.
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27. Gupta RK, Kesari AN, Murthy PS, Chandra R, Tandon V, Watal G.Hypoglycemic and antidiabetic effect of ethanolic extract of leaves of annona squamosa L. in experimental animals. J Ethnopharmacol 2005; 99:75–81.
27
28. Triender P. Determination of glucose in blood using glucose oxidase with an alternative oxygen acceptor. Ann Clin Biochem 1969; 6:24.
28
29. Farshchi A, Ghiasi G, Farshchi S, Malek Khatabi P. Effects of Boswellia papyrifera gum extract on learning and memory in mice and rats. Iran J Basic Med Sci 2010; 13:9-15.
29
30. Biessels GJ, Kamal A, Ramakers GM, Urban IJ, Spruijt BM, Erkelens DW, et al. Place learning and hippocampal synaptic plasticity in streptozotocin-induced diabetic rats. Diabetes 1996; 45: 1259–1266.
30
31. Biessels GJ, Kamal A, Urban IJ, Spruijt BM, Erkelens DW, Gispen WH, Water maze learning and hippocampal synaptic plasticity in streptozotocin-diabetic rats: effects of insulin treatment. Brain Res 1998; 800:125–135.
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34. Parale GP, Baheti NN, Kulkarni PM, Panchal NV. Effects of atorvastatin on higher functions. Eur J Clin Pharmacol 2006; 62:259–265.
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35. Raja SG, Dreyfus GD. Statins: much more than just a lipid lowering therapy. Indian Heart J 2004; 56:204–209.
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36. Masse I, Bordet R, Deplanque D, A1 Khedr A, Richard F , Libersa C, et al. Lipid lowering agents are associated with a slower cognitive decline in Alzheimer's disease. J Neurol Neurosurg Psychiatry 2005; 76:1624–1629.
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38. Chander R, Khanna AK, Pratap R. Antioxidant activity of guggulsterone, the active principle of guggulipid from Commiphora mukul. J Med Aromat Plant Sci 2002; 24:370–374.
38
ORIGINAL_ARTICLE
Effect of Curcumin on Doxorubicin-induced Cytotoxicity in H9c2 Cardiomyoblast Cells
Objective(s)
Doxorubicin (DOX), a widely used chemotherapeutic agent can give rise to serve cardiotoxicity by inducing apoptosis. Curcumin, the active compound of the rhizome of Curcuma longa L. has anti-inflammatory, antioxidant and anti-proliferative activities. Curcumin has been identified to increase cytotoxicity in several cancer cell lines in combination with DOX, but there is no study about its effect and DOX on normal cardiac cells. Therefore, in the present study, we evaluated the effect of curcumin on apoptosis induced by DOX in H9c2 rat heart-derived cells.
Materials and Methods
Cell viability was determined by MTT assay. Also, activation of caspase-3 was evaluated by spectrophotometry. Quantitative real time RT-PCR was used to evaluate the expression of c-IAP1. Detection of intracellular DOX accumulation was performed by flow cytometry.
Results
No toxicity observed when the cells exposed for 1 hr to different concentrations of curcumin, but pretreatment of cells with curcumin increased cytotoxicity of DOX in a dose dependent manner. Analysis of caspase-3 activation showed that curcumin pretreatment increased caspase-3 activation. RT-PCR analysis clearly showed that curcumin significantly decreased mRNA gene expression of c-IAP1 compared to cells treated with DOX alone. Pretreatment of H9c2 cells with DOX and curcumin had no effect on the intracellular accumulation of DOX.
Conclusion
Our observations indicated that subtoxic concentrations of curcumin sensitize H9c2 cells to DOX-induce apoptosis. These results suggest that the use of curcumin in combination with DOX in malignancy must be reevaluated.
https://ijbms.mums.ac.ir/article_4964_c94c71b2dcea6f49338dc35a67cfbdb2.pdf
2011-01-01
49
56
10.22038/ijbms.2011.4964
Apoptosis
Curcumin
Doxorubicin
H9C2 cells
Leila
Hosseinzadeh
hosinzadehl851@mums.ac.ir
1
Medical Toxicology Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Javad
Behravan
behravanj@ mums.ac.ir
2
Biotechnology Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Fatemeh
Mosaffa
3
Biotechnology Research Center, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Gholamreza
Bahrami
4
Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran
AUTHOR
Ahmad Reza
Bahrami
ar_bahrami@um.ac.ir
5
Faculty of Sciences, Ferdowsi University of Mashhad, Mashhad, Iran
AUTHOR
Gholamreza
Karimi
karimigh@mums.ac.ir
6
Medical Toxicology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
1. Tokarska-Schlattner M, Zaugg M, Zuppinger C, Wallimann T, Schlattner U. New insights into doxorubicininduced cardiotoxicity: The critical role of cellular energetics. J Mol Cell J Mol Cell 2006; 41:389-405.
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2. Wang S, Konorev EA, Kotamraju S, Joseph J, Kalivendi S, Kalyanaraman B. Doxorubicin induces apoptosis in normal and tumor cells via distinctly different mechanisms: Intermediacy of H2O2- and p53-dependent pathways. J Bioll Chem 2004; 279:25535-25543.
2
3. Spallarossa P, Garibaldi S, Altieri P, Fabbi P, Manca V, Nasti S, et al. Carvedilol prevents doxorubicin-induced free radical release and apoptosis in cardiomyocytes in vitro. J Mol Cell Cardiol 2004; 37:837-846.
3
4. Mizutani H, Tada-Oikawa S, Hiraku Y, Kojima M, Kawanishi S. Mechanism of apoptosis induced by doxorubicin through the generation of hydrogen peroxide. Life Sci 2005; 76:1439-1453.
4
5. Kim D-S, Woo E-R, Chae S-W, Ha K-C, Lee G-H, Hong S-T, et al. Plantainoside D protects adriamycininduced apoptosis in H9c2 cardiac muscle cells via the inhibition of ROS generation and NF-[kappa]B activation. Life Sci 2007; 80:314-323.
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6. Han X, Ren D, Fan P, Shen T, Lou H. Protective effects of naringenin-7-O-glucoside on doxorubicin-induced apoptosis in H9C2 cells. Eur J Pharmacol 2008; 581:47-53.
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7. Duvoix A, Blasius R, Delhalle S, Schnekenburger M, Morceau F, Henry E, et al. Chemopreventive and therapeutic effects of curcumin. Cancer Lett 2005; 223:181-190.
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8. Wang J,Du XX,Jiang H,Xie JX.Curcumin attenuates 6-hydroxydopamine-induced cytotoxicity by anti-oxidation and nuclear factor-kappaB modulation in MES23.5 cells. Biochem Pharmacol 2009; 78:178-183.
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9. Chen W, Zhao Z, Li L, Wu B, Chen Sf, Zhou H, et al. Hispolon induces apoptosis in human gastric cancer cells through a ROS-mediated mitochondrial pathway. Free Radic Biol Med 2008; 45:60-72.
9
10. Fiorillo C, Becatti M, Pensalfini A, Cecchi C, Lanzilao L, Donzelli G, et al. Curcumin protects cardiac cells against ischemia-reperfusion injury: effects on oxidative stress, NF-kB, and JNK pathways. Free Radic Biol Med 2008; 45:839-846.
10
11. Notarbartolo M, Poma P, Perri D, Dusonchet L, Cervello M, D'Alessandro N. Antitumor effects of curcumin, alone or in combination with cisplatin or doxorubicin, on human hepatic cancer cells. Analysis of their possible relationship to changes in NF-kB activation levels and in IAP gene expression. Cancer Lett 2005; 224:53-65.
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15. Spallarossa P, Fabbi P, Manca V, Garibaldi S, Ghigliotti G, Barisione C, et al. Doxorubicin-induced expression of LOX-1 in H9c2 cardiac muscle cells and its role in apoptosis. Biochem Biophys Res Commun 2005; 335:188- 196.
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16.Ortiz-Ortiz MA, Mor، أn JM, Bravosanpedro JM, Gonz، أlez-Polo RA, Niso-Santano M, Anantharam V, et al. Curcumin enhances paraquat-induced apoptosis of N27 mesencephalic cells via the generation of reactive oxygen species. Neurotoxicolgy 2009; 30:1008-1018.
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18. Bishnoi M, Chopra K, Kulkarni SK. Protective effect of curcumin, the active principle of turmeric (Curcuma longa) in haloperidol-induced orofacial dyskinesia and associated behavioural, biochemical and neurochemical changes in rat brain. Pharmacol Biochem Behav 2008; 88:511-522.
18
19. Choi BH, Kim CG, Lim Y, Shin SY, Lee YH. Curcumin down-regulates the multidrug-resistance mdr1b gene by inhibiting the PI3K/Akt/NF [kappa] B pathway. Cancer Lett 2008; 259:111-118.
19
20. Chuang SE, Yeh PY, Lu YS, Lai GM, Liao CM, Gao M, et al. Basal levels and patterns of anticancer druginduced activation of nuclear factor-kB (NF-kB), and its attenuation by tamoxifen, dexamethasone, and curcumin in carcinoma cells. Biocheml Pharmacol 2002; 63:1709-16.
20
21. Kunwar A, Sandur SK, Krishna M, Priyadarsini KI.Curcumin mediates time and concentration dependent regulation of redox homeostasis leading to cytotoxicity in macrophage cells. Euro J Pharmacol 2009; 611:8-16.
21
22. Garg S, Narula J, Chandrashekhar Y. Apoptosis and heart failure: clinical relevance and therapeutic target. J Mol Cell Cardiol 2005; 38:73-79.
22
23. Woo JH,Kim YH, Choi YJ,Kim DG, Lee KS, Bae JH, et al. Molecular mechanisms of curcumin-induced cytotoxicity: Induction of apoptosis through generation of reactive oxygen species, down-regulation of Bcl-X and IAP, the release of cytochrome c and inhibition of Akt. Carcinogenesis 2003; 24:1199-1212.
23
24. Karmakar S, Banik NL, Patel SJ, Ray SK. Curcumin activated both receptor-mediated and mitochondriamediated proteolytic pathways for apoptosis in human glioblastoma T98G cells. Neurosci Lett 2006; 407:53-62.
24
25. Zhang HZ, Yang L, Ren LM, Liu SM. Effects of curcumin combining with adriamycin to kill KB and KBv200 cells. Chin Pharmacol Bull 2001; 17:702-704.
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26. Thayyullathil F, Chathoth S, Hago A, Patel M, Galadari S. Rapid reactive oxygen species (ROS) generation induced by curcumin leads to caspase-dependent and -independent apoptosis in L929 cells. Free Radic Biolo Med 2008; 45:1403-1412.
26
27. Reuter S, Eifes S, Dicato M, Aggarwal BB, Diederich M. Modulation of anti-apoptotic and survival pathways by curcumin as a strategy to induce apoptosis in cancer cells. Biochem Pharmacol 2008; 76:340-351.
27
ORIGINAL_ARTICLE
Design of Agglomerated Crystals of Ibuprofen During Crystallization: Influence of Surfactant
Objective(s)
Ibuprofen is a problematic drug in tableting, and dissolution due to its poor solubility, hydrophobicity, and tendency to stick to surface. Because of the bad compaction behavior ibuprofen has to be granulated usually before tableting. However, it would be more satisfactory to obtain directly during the crystallization step crystalline particles that can be directly compressed and quickly dissolved.
Materials and Methods
Crystallization of ibuprofen was carried out using the quasi emulsion solvent diffusion method in presence of surfactant (sodium lauryl sulfate (SLS), Tween 80). The particles were characterized by differential scanning calorimetry (DSC), powder X-ray diffraction (XRPD) and were evaluated for particle size, flowability, drug release and tableting behavior.
Results
Ibuprofen particles obtained in the presence of surfactants consisted of numerous plate- shaped crystals which had agglomerated together as near spherical shape. The obtained agglomerates exhibited significantly improved micromeritic properties as well as tableting behavior than untreated drug crystals. The agglomerates size and size distribution was largely controlled by surfactant concentration, but there was no significant influence found on the tableting properties. The dissolution tests showed that the agglomerates obtained in presence of SLS exhibited enhanced dissolution rate while the agglomerates made in the presence of Tween 80 had no significant impact on dissolution rate of ibuprofen in comparison to untreated sample. The XRPD and DSC results showed that during the agglomeration process, ibuprofen did not undergo any polymorphic changes.
Conclusion
The study highlights the influence of surfactants on crystallization process leading to modified performance.
https://ijbms.mums.ac.ir/article_4965_1a5b9607b0d34c08ad089dedd14a4b41.pdf
2011-01-01
57
66
10.22038/ijbms.2011.4965
Direct compression
Emulsion solvent diffusion method
Ibuprofen
Surfactant
Maryam
Maghsoodi
mmaghsoodi@ymail.com
1
Drug applied Research Center, School of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
Leila
Barghi
2
School of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
1. York P. Crystal engineering and particle design for the powder compaction process .Drug Dev Ind Pharm 1992; 18:677.
1
2. York P, Shekunov BYu. Crystallization processes in pharmaceutical technology and drug delivery design. J Cryst Growth 2000; 211:122-136.
2
3. Rasenack N, Muller B. Crystal habit and tableting behavior of ibuprofen. Int J Pharm 2002; 244:45–57.
3
4. Rasenack N, Muller B. Ibuprofen crystal with optimized properties. Int J Pharm 2002; 245:9–24.
4
5. Khan MA, Bolton S, Kislalioglu MS. Optimization of process variables for the preparation of ibuprofen coprecipitates with Eudragit S100. Int J Pharm 1994; 102:185-192.
5
6. Kachrimanis K, Ktistis G, Malamataris S. Crystallization conditions and physicochemical properties of ibuprofen- Eudragit†S100 spherical crystal agglomerates prepared by the solvent-change technique. Int J Pharm 1998; 173:61-74.
6
7. Pawar A, Paradkar A, Kadam Sh, Mahadik K. Agglomeration of Ibuprofen with Talc by Novel Crystallo-Co- Agglomeration Technique. AAPS PharmSciTech 2004; 5: Article 55.
7
8. Carr RL. Evaluation flow properties of solids. Chem Eng 1965; 72:163-168.
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9. Carr RL. Classifying flow properties of solids. Chem Eng 1965; 72:69-72.
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10. Fell JT, Newton JM. Determination of tablet strength by the diametral- compression test. J Pharm Sci 1970; 59:688–691.
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11. Joiris E, Di Martino P, Berneron C, Guyot-Hermann AM, Guyot JC. Compression behavior of orthorhombic paracetamol. Pharm Res 1998; 15:1122-1130.
11
12. Rasenack N, Muller BW. Ibuprofen crystals with optimized properties. Int J Pharm. 2002; 245:9-24.
12
13. Verma S, Gokhaleb R, Burgessa DJ. A comparative study of top-down and bottom-up approaches for the preparation of micro/nanosuspensions. Int J Pharm 2009; 380:216–222.
13
14. Jbiilou M, Ettabia A, Guyot-Harmann AM, Guyot JC. Ibuprofen agglomerates preparation by phase separation. Drug Dev Ind Pharm 1999; 25:297-305.
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15. Eriksson M, Alderborn G. The effect of the original particle size and tablet porosity on the increase in tensile strength during storage of sodium chloride tablets in a dry atmosphere. Int J Pharm 1995; 113:199-207.
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16. Kawashima Y, Imai M, Takeuchi H, Yamamoto H, Kamiya K, Hino T. Improved flowability and compactability of spherically agglomerated crystals of ascorbic acid for direct tableting designed by spherical crystallization process. Adv Powder Technol 2003; 130:283–289.
16
17. Nokhodchi A, Maghsoodi M, Hassan-Zadeh D, Barzegar-Jalali M. Preparation of agglomerated crystals for improving flowability and compactibility of poorly flowable and compactible drugs and excipients. Adv Powder Technol 2007; 175:73–81.
17
18. Maghsoodi M, Taghizadeh O, Martin GP, Nokhodchi A. Particle design of naproxen-disintegrant agglomerates for direct compression by a crystallo-co-agglomeration technique. Int J Pharm 2008; 35:45–54.
18
19. Szabo RP, Goczo H, PintyeHodi K, Kasajr P, Eros I , HasznosNezdei M, et al. Development of spherical crystals of an Aspartic acid salt for direct tablet making. Adv Powder Technol 2001; 114:118-24.
19
20. Paradkar AR, Pawar AP, Chordiya J K, Patil VB, Ketkar AR. Spherical crystallization of celecoxib. Drug Dev Ind Pharm 2002; 28:1213-1220.
20
21. Eriksson M, Alderborn G. The effect of particle fragmentation and deformation on the interparticulate bond formation process during powder compaction. Pharm Res 1995; 12:1031–1039.
21
22. Rasenack N, Muller B. Crystal habit and tableting behavior of ibuprofen. Int J Pharm 2002; 244:45–57.
22
23. Maheshwari M, Jahagirdar H, Paradkar A. Melt sonocrystallization of ibuprofen: Effect on crystal properties. Eur J Pharm Sci 2005; 25:41–48.
23
24. Garekani HA, Sadeghi F, Badiee A, Mostafa SA, Rajabi-Siahboomi AR. Crystal habit modifications of ibuprofen and their physicomechanical characteristics. Drug Dev Ind Pharm 2001; 27:803–809.
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25. El-Said Y. Effect of Co-solvents on water content and physical properties of acetaminophen crystallized from aqueous solutions. STP Pharm Sci 1995; 5:232-237.
25
26. Nokhodchi A, Bolourchian N, Dinarvand R. Crystal modification of phenytoin using different solvents and crystallization conditions. Int J Pharm 2003; 250:58-97.
26
ORIGINAL_ARTICLE
Effect of Matricaria aurea (Loefl.) Shultz-Bip. Hydroalcoholic Extract on Acetic Acid-Induced Acute Colitis in Rats
Objective(s)
Matricaria aurea is found abundant in Iran and has large similarities in constituents especially essential oils, flavones and flavonoides as well as traditional uses to the main species; Matricaria recutita L. Anti-inflammatory, antioxidant and spasmolytic properties of the main species suggest that this plant may have beneficial effects on inflammatory bowel diseases so the present study was carried out.
Materials and Methods
Hydroalcoholic extract of plant with doses of 200, 400, 800 mg/kg were administered orally (p.o.) for 5 days and rectally (i.r.) (400 and 800 mg/kg) at 15 and 2 hr before ulcer induction. To induce colitis, 2 ml of acetic acid 4% was instilled intra-colonically to separate groups of male Wistar rats (n= 6). Normal saline (2 ml), prednisolone (4 mg/kg) and hydrocortisone acetate (20 mg/kg) enema were administered to control and reference groups respectively. The tissue injures were assessed macroscopically and histopathologically.
Results
Greater doses of extract (400 and 800 mg/kg) reduced colon weight/length ratio (P< 0.01) and the highest test dose (800 mg/kg p.o. or i.r.) was effective to decrease tissue damage parameters including ulcer severity, area and index (P< 0.01) as well as inflammation severity and extent, crypt damage and total colitis index (P< 0.01) significantly.
Conclusion
It is concluded that Matricaria aurea extract was effective to protect against acute colitis in acetic acid model and this effect was more significant with the greater doses administered orally or rectally. Further studies are warranted to ascertain the mechanisms that are involved and the responsible active constituents.
https://ijbms.mums.ac.ir/article_4966_74b7aa6e8338ad642c2bd30658780140.pdf
2011-01-01
67
74
10.22038/ijbms.2011.4966
Acetic acid
Experimental colitis
Matricaria aurea
Plant extract
Rats
Mohsen
Minaiyan
minaiyan@pharm.mui.ac.ir
1
Department of Pharmacology and Isfahan Pharmaceutical Sciences Research Center, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
LEAD_AUTHOR
Nasrollah
ghassemi-Dehkordi
2
Department of Pharmacognosy, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Parvin
Mahzouni
3
Department of Clinical Pathology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
AUTHOR
Meysam
Ansari-Roknabady
4
AUTHOR
1. McKay DL, Blumberg JB. A review of bioactivity and potential health benefits of chamomile tea (Matricaria recutita L.). Phytother Res 2006; 20:519-530.
1
2. Ghassemi-Dehkordi N. Matricaria. In: Iranian Herbal Pharmacopoeia Scientific Committee, editors, Iranian Herbal Pharmacopeia. 1st ed. Tehran: Iran Ministry of Health & Medical Education Publications; 2002. p. 99- 107.
2
3. Ahmed AA, Abou Elela MA. Highly oxygenated bisabolenes and an acetylene from Matricaria aurea. Phytochemistry 1999; 51:551-554.
3
4. Ali-Shtayeh M, Yaniv Z, Mahajna J. Ethnobotanical survey in the Palestinian area. A classification of the healing potential of medicinal plants. J Ethnopharmacol 2000; 73: 221-232.
4
5. Capasso F, Grandolini G. Fitofarmacia. 2nd ed. Milan: Springer Veralg; 1999.
5
6. Al-Mustafa AH, Al-Thonibat OY. Antioxidant activity of some Jordanian medicinal plants used traditionally for treatment of diabetes. Pak J Biol Sci 2008; 11:351-358.
6
7. Sartor RB. Pathogenesis and immune mechanism of chronic inflammatory bowel diseases. Am J Gastroenterol 1997; 92:5S-11S.
7
8. Brzezinski A. Inflammatory bowel diseases. In: Andreoli TE, Carpenter CCJ,Griggs RC, Loscalzo TE, editors. Cecil essentials of medicine. 5th ed. Philadelphia:Saunders WB Company; 2001.
8
9. Lih-Brody L, Powell SR, Collier KP, Reddy GM, Cerchia R, Kahn E, et al. Increased oxidative stress and decreased antioxidant defences in mucosa of inflammatory bowel disease. Dig Dis Sci 1996; 41:2078-2086.
9
10. Bouma C, Strober W. The immunological and genetic basis of inflammatory bowel disease. Nat Rev Immunol 2003; 3:521-533.
10
11. Mascolo N, Izzo A, Autore G, Maiello F, Dicarlo G, Capsso F. Acetic acid-induced colitis in normal and essential fatty acid deficient rats. J Pharmacol Exp Ther 1995; 272:469- 475.
11
12. Morris GP, Beck PL, Herridge MS, Depew WT, Szewczuck MR, Wallace JL. Hapten induced model of inflammation and ulceration in rat colon. Gastroenterology 1989; 96:795-803.
12
13.Minaiyan M, Ghannadi AR, Karimzadeh A.Antiulcerogenic effects of ginger (Zingiber officinale Roscoe) on cysteamine induced duodenal ulcer in rats. DARU 2006; 14:97-101.
13
14. Vogel HG, Vogel WH. Drug discovery and evaluation (Pharmacological Assays). 2nd ed. Berlin: Springer Verlag;1997.
14
15. Minaiyan M, Ghannadi A, Mahzouni P, Nabi-Meibodi. Anti-ulcerogenic effect of ginger (rhizome of Zingiber officinale Roscoe) hydroalcoholic extract on acetic acid- induced acute colitis in rats. Res Pharm Sci 2008; 3:15-22.
15
16. Cooper HS, Murthy SNS, Shah RS, Sedergran DJ. Clinicopathologic study of dextran sulfate sodium experimental murine colitis. Lab Invest 1993; 69:238-249.
16
17. Dieleman LA, Palmen MJHJ, Akol H, Bloemena E, Pena AS, Meuwissen SGM. Chronic experimental colitis induced by dextran sulfate sodium (DSS) is characterized by Th1 and Th2 cytokines. Clin Exp Immunol 1998; 114:385-391.
17
18. MacPherson BR, Pfeiffer CJ. Experimental production of diffuse colitis in rats. Digestion 1978; 17:135-150.
18
19. Mahgoub AA, El-Medany AH, Hagar HH, Sabah DM. Protective effect of natural honey against acetic acidinduced colitis in rats. Trop Gastroenterol 2002; 23:82-87.
19
20. Paiva LA, Gurgel LA, De Sousa ET, Silveria ER, Silva RM, Santos FA, et al. Protective effect of Copaifera langsdorffii oleo-resin against acetic acid-induced colitis in rats. J Ethnopharmacol 2004; 93:51-56.
20
21. Evans WC. Trease and evance pharmacognosy. 15th ed. Edinburgh: Saunders WB; 2002.
21
22. Khayyal MT, El-Ghazaly MA, Kenawy SA, Seif-El-Nasr M, Mahran LG, Kafafi YA, et al. Antiulcerogenic effect of some gasterointestinally acting plant extracts and their combinations. Arzneimittelforschung 2001; 51:545-553.
22
23. Gholami A, Aboulhasani Z, Mohagheghzadeh A. Treatment of gastric ulcer by herbal medicine. In: Ebadi M, editor. Pharmacodynamic basis of herbal medicine. 1st ed.Tehran: Rahe Kamal Press Inc; 2007. p. 933-943.
23
24. Tan PV, Njimi CK, Ayafor JF. Screening of some African medicinal plants for antiulcerogenic activity: part 1. Phytother Res 1997; 11:45-47.
24
25. Borelli F, Izzo AA. The plant kingdom as a source of antiulcer remedies. Phytother Res 2000; 14:581-591.
25
26. El-Abhar HS, Hammad LN, Gawad HS. Modulating effects of ginger extract on rats with ulcerative colitis. J Ethnopharmacol 2008; 118:367-372.
26
27. Jagtap AG, Shirke SS, Phadke AS. Effect of polyherbal formulation on experimental models of inflammatory bowel diseases. J Ethnopharmacol 2004; 90:195-204.
27
ORIGINAL_ARTICLE
Effects of Chronic Oral Administration of Natural Honey on Ischemia/Reperfusion-induced Arrhythmias in Isolated Rat Heart
Objective(s)
In this study, effects of chronic administration of oral natural honey against ischemia/reperfusion (I/R)- induced cardiac arrhythmias were investigated in isolated rat heart.
Materials and Methods
Male Wistar rats were divided into four groups (n= 10-14 rats in each group) and fed with natural honey (1%, 2% and 4% dissolved in the drinking water) for 45 days except for the control group. After anesthesia, the rats’ hearts were isolated quickly, mounted on a Langendorff apparatus and perfused with a modified Krebs-Henseleit solution during stabilization, 30 min regional ischemia followed by 30 min reperfusion. The ECGs were recorded throughout the experiments to analyze cardiac arrhythmias based on the Lambeth conventions.
Results
In the ischemic phase, honey (1%) significantly reduced (P<0.05) the number and duration of ventricular tachycardia (VT). Honey (1% and 2%) also significantly decreased number of ventricular ectopic beats (VEBs). In addition, incidence and duration of reversible ventricular fibrillation (Rev VF) were lowered by honey 2% (P<0.05). During reperfusion time, VT incidence was 73% in the control group, however natural honey (1%) decreased it to 22% (P<0.05). Honey also produced significant reduction in the incidences of total VF, Rev VF, duration and number of VT.
Conclusion
For the first time, the results of present study demonstrated protective effects of chronic oral honey administration against I/R-induced arrhythmias in isolated rat heart. Antioxidant activity, the existence of energy sources such as glucose and fructose and improvement of some hemodynamic functions might be responsible for these effects.
https://ijbms.mums.ac.ir/article_4967_56e373762d43538d6bea7fa1c2768c92.pdf
2011-01-01
75
81
10.22038/ijbms.2011.4967
Arrhythmia
Honey
Ischemia
Rat
Reperfusion
Moslem
Najafi
najafim@tbzmed.ac.ir
1
Department of Pharmacology, School of Pharmacy and Research Center for Pharmaceutical Nanotechnology, Tabriz University of Medical Sciences, Tabriz, Iran
LEAD_AUTHOR
Elnaz
Shaseb
2
School of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Saba
Ghaffary
3
School of Pharmacy, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Ashraf
Fakhrju
4
Department of Pathology, School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
Tahereh
Eteraf Oskouei
eteraf_t@yahoo.com
5
School of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
AUTHOR
1. Zheng ZJ, Croft JB, Giles WH, Mensah GA. Sudden cardiac death in the United States, 1989 to 1998.
1
Circulation 2001; 104:2158–2163.
2
2. Selwyn AP, Braunwald E. Ischemic heart diseases. In: Kasper LD, Fauci SA, editors. Harrison’s Principles of Internal Medicine. 16th ed. New York: The Mc Graw- Hill companies; 2004. p.1435- 1444.
3
3. Lango R, Smolenski RT, Narkiewicz M, Suchorzewska J, Lysiak-Szydlowska W. Influence of L-carnitine and its derivatives on myocardial metabolism and function in ischemic heart disease and during cardiopulmonary bypass. Cardiovasc Res 2001; 51:21-29.
4
4. Ford DA. Alterations in myocardial lipid metabolism during myocardial ischemia and reperfusion. Prog Lipid Res 2002; 41:6-26.
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5. Rizzon P, Biasco G, Di Biase M, Boscia F, Rizzo U, Minafra F, et al. High doses of L-carnitine in acute myocardial infarction: metabolic and anti-arrhythmic effects. Eur Heart J 1989; 10:502-508.
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6. Codex A limentarius Commission, author. Codex Standards for sugar (honey). Supplement 2 to codex Alimentarius, Volume 111. Rome: Food and Agriculture Organisation of the United Nations and World Health Organization; 1989.
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7. Moundoi MA, Padila-Zakour OI, Worobo RW. Antimicrobial activity of honey against food pathogens and food spoilage microorganisms. Geneva: Cornell University, NYSAES; 2001. Vol. 1 p. 61–71.
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8. Olaitan PB, Adeleke EO, Ola OI. Honey: a reservoir for microorganisms and an inhibitory agent for microbes. Afr Health Sci 2007; 7:159–165.
9
9. Ahmed AK, Hoekstra MJ, Hage JJ, Karim RB. Honey-medicated dressing: transformation of an ancient remedy into modern therapy. Ann Plast Surg 2003; 50:143-147.
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10. Ali AT, Chowdhury MN, al Humayyd MS. Inhibitory effect of natural honey on Helicobacter pylori. Trop Gastroenterol 1991; 12:139-143.
11
11. Molan PC. The antibacterial activity of honey: The nature of the antibacterial activity. Bee World 1992; 73:5–28.
12
12. Khan FR, Ul Abadin Z, Rauf N. Honey: nutritional and medicinal value. Int J Clin Pract 2007; 61:1705-1707.
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13. Asadi-Pooya A, Pnjehshahin MR, Beheshti S. The antimycobacterial effect of honey: an in vitro study. Riv Biol 2003; 96: 491-496.
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14. Johnson DW, Eps CV, Mudge DW, Joan Wiggins K, Armstrong K, Hawley CM, et al. Randomized, controlled trial of topical exit-site application of honey versus mupirocin for the prevention of catheter-associated infections in hemodialysis patients. J Am Soc Nephrol 2005; 16: 1456–1462.
15
15. Gheldof N, Wang XH, Engeseth NJ. Identification and quantification of antioxidant components of honeys from various floral sources. J Agric Food Chem 2002; 50:5870-5877.
16
16. Baltrusˇaityt V, Venskutonis PR, Cˇ eksteryt V. Radical scavenging activity of different floral origin honey and beebread phenolic extracts. Food Chem 2007; 101:502–514.
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17. Gheldof N, Wang XH, Engeseth NJ. Buckwheat honey increases serum antioxidant capacity in humans. J Agric Food Chem 2003; 51:1500-1505.
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18. Hegazi AG, Abd El-Hady FK. Influence of honey on the suppression of human low density lipoprotein (LDL) peroxidation (In vitro). Evid Based Complement Alternat Med 2009; 6:113-121.
19
19. Beretta G, Orioli M, Facino RM. Antioxidant and radical scavenging activity of honey in endothelial cell cultures. Planta Med 2007; 73:1182-1189.
20
20. Rakha MK, Nabil IZ, Hussein AA. Cardioactive and vasoactive effects of natural wild honey against cardiac malperformance induced by hyperadrenergic activity. J Med Food 2008; 11:91–98.
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21. Schramm DD, Karim M, Schrader HR, Holt RR, Cardetti M, Keen CL. Honey with high levels of antioxidants can provide protection to healthy human subjects. J Agric Food Chem 2003; 51: 1732-1735.
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22. Chepulis LM. The effect of honey compared to sucrose, mixed sugars, and a sugar-free diet on weight gain in young rats. J Food Sci 2007; 72: S224-S229.
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23. Bahrami M, Ataie-Jafari A, Hosseini S, Forouzanfar M, Rahmani M, Pajouhi M. Effects of natural honey consumption in diabetic patients: an 8-week randomized clinical trial. Int J Food Sci Nutr 2008; 2: 1-9.
24
24. Yaghoobi N, Al-Waili N, Ghayour-Mobarhan M, Parizadeh SMR, Abasalti Z, Yaghoobi Z, et al. Natural honey and cardiovascular risk factors; effects on blood glucose,cholesterol, triacylglycerole, CRP, and body weight compared with sucrose. Scientific World Journal 2008; 8: 463-469.
25
25. Al-Waili NS. Natural honey lowers plasma glucose, C-reactive protein, homocysteine, and blood lipids in healthy, diabetic, and hyperlipidemic subjects: comparison with dextrose and sucrose. J Med Food 2004; 7:100-107.
26
26. Najafi M, Mahdizadeh-Aghdam E, Rafie F, Eteraf Oskouei T. Effects of pharmacologic preconditioning by natural honey on arrhythmias and infarct size in isolated heart, Pharm Sci J 2008; 1-11.
27
27. Najafi M, Garjani A. The effect of L-carnitine on arrhythmias in the ischemic rat heart. Iran J Basic Med Sci 2005; 8:38-44.
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28. Kristiansen SB, Nielsen–Kudsk JE, Botker HE, Nielsen TT. Effects of KATP channel modulation on myocardial glycogen content, lactate and amino acids in non-ischemic and ischemic rat hearts. J Cardiovasc Pharmacol 2005; 45:456–461.
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29. Najafi M, Garjani A, Maleki N, Eteraf Oskouei T. Antiarrhythmic and arrhythmogenic effects of L-carnitine in ischemia and reperfusion. Bull Exp Biol Med 2008; 146:210-213.
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30. Najafi M, Nazemiyeh H, Ghavimi H, Gharakhani A, Garjani A. Effects of hydroalcoholic extract of Cynodon dactylon (L.) pers. on ischemia/reperfusion-induced arrhythmias. DARU 2008; 16:233-238.
31
31. Najafi M, Garjani A, Eteraf Oskouei T. Comparison between the effects of ischemic preconditioning and pharmacologic preconditioning by L-carnitine on infarct zone size in the ischemic-reperfused isolated rat heart. Iran J Basic Med Sci 2007; 10:54-59.
32
32. Chow J. Probiotics and prebiotics: a brief overview. J Ren Nutr 2002; 12:76-86.
33
33. White JW. Composition of honey. In: Crane E, editor. Honey: A Comprehensive Survey, London: Heinemann; 1979. p. 157–192.
34
34. Bilsel Y, Bugra D, Yamaner S, Bulut T, Cevikbas U, Turkoglu U. Could honey have a place in colitis therapy? Effects of honey, prednisolone and disulfiram on inflammation, nitric oxide, and free radical formation. Dig Surg 2002; 19:306-311.
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35. Zalibera M, Stasko A, Slebodova A, Jancovicova V, Cermakova T, Brezova A. Antioxidant and radical-scavenging activities of Slovak honeys – An electron paramagnetic resonance study. Food Chem 2008; 110:512–521.
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36. Shimazawa M, Chikamatsu S, MorimotoN, Mishima S, Nagai H, Hara H. Neuroprotection by Brazilian Green Propolis against in vitro and in vivo ischemic neuronal damage. Evid Based Complement Alternat Med 2005; 2:201–207.
37
ORIGINAL_ARTICLE
The Effect of Linear PEI on Characteristics and Transfection Efficiency of PEI-Based Cationic Nanoliposomes
The development of efficient and safe carrier system to transfer DNA into cells is essential in non-viral gene therapy. The aim of the present study was to evaluate the effect of linear polyetheneimine (lPEI) (2500 Da) on the physicochemical and biological properties of lipopolyplexes constructed from liposomes and lPEI.
Materials and Methods
Different lipopolymers were synthesized from lPEI and acrylate derivatives. Nanocarriers were composed of the lipids (DOPE, DPPE and DOTAP) and the synthesized lipopolymers. After characterization of the prepared vectors by determination of size and zeta potential, transfection activity was tested in Neuro2A cells. Ethidium bromide and MTT test were used to evaluate the DNA condensation ability and cytotoxicity of vectors, respectively.
Results
Vector’s size ranged from 95 to 337 nm and they had positive charge. The differences in DNA binding properties of lipopolyplexes were not significant. Among lipids, DOTAP showed better impact on transfection efficiency. The highest transfection activity was achieved by liposomal formulation consist of DOTAP and lipopolymer composed of lPEI and hexyl acrylate. The lipopolyplexes showed minimum cytotoxicity to the cultured cells in vitro.
Conclusion
The results of study confirmed that it is possible to improve gene expression using lipopolyplexes.
https://ijbms.mums.ac.ir/article_4968_c0f2cd5169341147dcd51c5ae9ade086.pdf
2011-01-01
82
88
10.22038/ijbms.2011.4968
Acrylates
Gene transfer
Linear polyethyleneimine
Liposomes
Mohammad
Ramezani
m.ramazani@mums.ac.ir
1
Pharmaceutical Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Bizhan
Malaekeh-Nikouei
malaekehb@mums.ac.ir
2
Nanotechnology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Tahreh
Khakshoor
3
Nanotechnology Research Centre, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mohammad
Malaekeh-Nikouei
4
Pharmaceutical Research Centre, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
1. El-Aneed A. An overview of current delivery systems in cancer gene therapy. J Control Release 2004; 94:1-14.
1
2. Garcia L, Bunuales M, Duzgunes N, Tros de Ilarduya C. Serum-resistance lipopolyplexes for gene delivery to liver tumour cells. Eur J Pharm Biopharm 2007; 67:58-66.
2
3. Matsumoto M, Kishkawa R, Kurosaki T, Nakagawa H, Ichikawa N, Hamamoto T, et al. Hybrid vector including polyethylenimine and cationic lipid, DOTMA, for gene delivery. Int J Pharm 2008; 363:58-65.
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4. Gao X, Kim K, Liu D. Nonviral gene delivery:What we know and what is next. AAPS J 2007; 9:E92-104.
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5. Luo D, Saltzman WM. Synthetic DNA delivery systems. Nat Biotechnol 2000; 18:33-37.
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6. Elouahabi A, Ruysschaert J. Formation and intracellular trafficking of lipoplexes and polyplexes. Mol Ther 2005; 11:336-347.
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7. Khalil IA, Kogure K, Akita H, Harashima H. Uptake pathways and subsequent intracellular trafficking in nonviral gene delivery. Pharmacol Rev 2006; 58:32-45.
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8. Chen J, Wang H, Gao J, Chen H, Liang W. Liposomes modified with polycation used for gene delivery: Preparation, characterization and transfection in vitro. Int J Pharm 2007; 343:255-261.
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9. McNeil SE, Perrie Y. Gene delivery using cationic liposomes. Expert Opin Ther Pat 2005; 16:1371-1382.
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10. Hanzlikova M, Soinine P, Lampela P, Mannisto PT, Raasmaja A. The role of PEI structure and size in the PEI/liposome-mediated synergism of gene transfection. Plasmid 2009; 61:15-21.
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11. Yamazaki Y, Nango M, Matsuura M, Hasegawa Y, Hasegawa Y, Oku N. Polycation liposomes, a novel nonviral gene transfer system, constructed from cetylated polyethylenimine. Gene Ther 2000; 7:1148-1155.
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12. Merdan T, Kopecek J, Kissel T. Prospects for cationic polymers in gene and oligonucleotide therapy against cancer. Adv Drug Deliv Rev 2002; 54:715-758.
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13. Lee C, Ni Y, Chen C, Chou C, Chang F. Synergistic effect of polyethylenimine and cationic liposmes in nucleic acid delivery to human cancer cells. Biochim Biophys Acta 2003; 1611:55-62.
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14. Masotti A, Moretti F, Mancini F, Russo G, Di Lauro N, Checchia P, et al. Physicochemical and biological study of selected hydrophobic polyethylenimine-based polycationic liposomes and their complexes with DNA. Bioorg Med Chem 2007; 15:1504-1515.
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15. Ko YT, Kale A, Hartner WC, Papahadjopoulos-Sternberg B, Torchilin VP. Self-assembling micelle-like nanoparticles based on phospholid-polyethyleneimine conjugates for systemic gene delivery. J Control Release 2009; 133:132-138.
15
16. Malaekeh-Nikouei B, Malaekeh-Nikouei M, Kazemi Oskuee R, Ramezani M. Preparation, characterization and transfection efficiency of nanoliposomes modified with oligoamines as gene carrier. Nanomedicine:NBM 2009; 5:457-462.
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17. Zintchenko A, Philipp A, Dehshahri A, Wagner E. Simple modifications of branched PEI lead to highly efficient siRNA carriers with low toxicity. Bioconjug Chem 2008; 19:1448-1455.
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18. Lampela P, Elomaa M, Ruponen M, Urtti A, Mannisto PT, Raasmaja A. Different synergistic roles of small polyethylenimine and Dosper in gene delivery. J Control Release 2003; 88:173-178.
18
19. Incani V, Tunis E, Clements BA, Olson C, Kuchavski C, Lavasanifar A, et al. Palmetic acid substitution on cantianic polymers for effective delivery of plasmid DNA to bone marrow stromal cells. Biomed Mater Res 2006; 81:493-504.
19
20. Zuhorn IS, Bakowsky U, Polushkin E, Visser WH, Marc CA, Stuart J, et al. Nonbilayer phase of lipoplex– membrane mixture determines endosomal escape of genetic cargo and transfection efficiency. Mol Ther 2005, 11:801-810.
20
21. Ramezani M, Khoshhamdam M, Dehshahri A, Malaekeh-Nikouei B. The influence of size, lipid composition and bilayer Tm on the transfection efficiency of nanolipoplexes. Colloids Surf B 2009; 72:1 5.
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22. Simões S, Filipe A, Faneca H, Mano M, Penacho N, Düzgünes N, et al. Cationic liposomes for gene delivery. Expert Opin Drug Deliv 2005; 2:237-254.
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23. Godbey WT, Wu KK, Mikos AG. Polyethyleneimine and its role in gene delivery. J Control Release 1999; 60:149-160.
23
24. Fischer D, Bieber T, Li Y, Elsasser HP, Kissel T. A novel non-viral vector for DNA delivery based on low molecular weight. Pharm Res 1999; 17:1373-1379.
24
ORIGINAL_ARTICLE
The Effect of MS14 on Production of Pro-inflammatory Cytokines by Macrophages
Objective(s)
Using herbal medicines as a complementary treatment method is increasing in wide variety of diseases. MS14-an herbal-marine preparation-is reported to have anti-inflammatory and immunomodulatory activities; however, the mechanism underlying its therapeutic effect is not known. Macrophages play an important role in host defense mechanisms and carry out their role by producing various mediators including proinflammatory cytokines (TNFα, IL-1β). In this study the effects of orally administered MS14 on TNFα and IL-1β production of BALB/c mice peritoneal macrophages were evaluated.
Materials and Methods
MS14 at 100 mg/kg was orally administered for 5 days to BALB/c mice in MS14 group. Sterile normal
saline was administered to mice in control group. Peritoneal macrophage were isolated from control and MS14 groups and cultured, then the supernatants were collected and the cytokines IL-1β and TNFα were measured by ELISA test.
Results
Significant decrease in TNFα and IL-1β production of macrophages both at the presence and absence of stimulators was observed. TNFα levels were 64.7±4.6 and 51.1±4.2 pg/ml in drug and control groups respectively (P< 0.05) and 298.7±31.3 and 177.0±26.5 pg/ml in stimulated (PMA+fMLP) cultures of drug and control groups respectively (P< 0.007). The IL-1β levels was 130.1±2.8 pg/ml in control and 65.1±5.6 in MS14 group (P< 0.000).
Conclusion
It could be concluded that MS14 is able to cause a decline in some inflammatory responses of immune system, which could be considered as at least one of its immunomodulatory mechanisms.
https://ijbms.mums.ac.ir/article_4969_24a86427859fb75f3e275fd5e733fd23.pdf
2011-01-01
89
93
10.22038/ijbms.2011.4969
BALB/c mice
Interleukin-1beta (IL-1β)
Macrophages
MS14
Tumor necrosis factor-alpha
(TNFα)
Roya
Yaraee
ryaraee@yahoo.com
1
Department of Immunology, Medical School and Medicinal Plant Research Center, Shahed University, Tehran, Iran
LEAD_AUTHOR
Nayere
Askari
2
Department of biology, faculty of Basic Sciences, Shahid Bahonar University, Kerman, Iran
AUTHOR
Mohsen
Naseri
naseri@shahed.ac.ir
3
Department of Pharmacology and Department of Iranian Traditional Medicine, Medical School, Shahed University, Tehran, Iran
AUTHOR
1. Choi CY, Kim JY, Kim YS, Chung YC, Seo JK, Jeong HG. Aqueous extract isolated from Platycodon grandiflorum elicits the release of nitric oxide and tumor necrosis factor- a frommurine macrophages. Int Immunopharmacol 2001; 1:1141–1151.
1
2. Cope AP. Regulation of autoimmunity by proinflammatory cytokines. Curr Opin Immunol 1998; 10:669-676.
2
3. Iorioa AD, Ferruccib L, Sparvieria E, Cherubinic A,Volpatod S, Corsib A, et al. Serum IL-1b levels in health and disease:a population-based study. InCHIANTI study. Cytokine 2003; 22:198–205.
3
4. Werner GH, Jolles P.Immunstimulating agent:what next? Eur J Biochem 1996; 242:1-19.
4
5. Henderson L,Yue QY, Bergquist C, Gerden B, Arlett P. St John’s wort (Hypericum perforatum): drug interactions and clinicaloutcomes. Br J Clin Pharmacol 2002; 54: 349–356.
5
6. Naseri M, Ahmadi A, Ghareghozli K, Nabavi M, Faghiehzade S, Ashtarian N. Clinical and toxicitology evaluation of MS14 natural product in patients with Multiple sclerosis. Daneshvar 2007; 68:59-64.
6
7. Tafreshi AP, Ahmadi A, Ghaffarpur M, Mostsfavi H, Rezaeizadeh H, Minaie B, et al. An Iranian herbal-marine medicine, MS14, ameliorates experimental allergic encephalomyelitis. Phytother Res 2008; 22:1083-1086.
7
8. Hajhashemi V, Ghafghazi T, Ahmadi A. Investigation of subacute toxicity of MS14 natural drug in rat. Daneshvar 2004; 11:11-14.
8
9. Tripathi S, Bruch D, Kittur DS. Ginger extract inhibits LPS induced macrophage activation and function. BMC Complement Alter Med 2008; 8:1.
9
10. Kim SJ, Jeong H-J, Moon PD, Lee L, Jung HJ, et al. Anti-inflammatory activity of gumiganghwaltang through the inhibition of nuclear factor- kB activation in peritoneal macrophages. Biol Pharm Bull 2005; 28:233-237.
10
11. O'Connor JC, McCusker RH, Strle K, Johnson RW, Dantzer R, Kelley KW. Regulation of IGF-I function by proinflammatory cytokines: at the interface of immunology and endocrinology. Cell Immunol 2008; 252:91-110.
11
12. Brennan FM, McInnes IB. Evidence that cytokines play a role in rheumatoid arthritis. J Clin Invest 2008; 118:3537-3545
12
13. Anolik JH. B cell biology and dysfunction in SLE. Bull NYU Hosp Jt Dis 2007; 65:182-186.
13
14. Imitola J, Chitnis T, Khoury S. Cytokines in multiple sclerosis: from bench to bedside. Pharmacol Ther 2005; 106:163-177.
14
15. Calixto JB, Campos MM, Otuki MF, Santos AR. Anti-inflammatory compounds of plant origin. Part II. Modulation of pro-inflammatory cytokines, chemokines and adhesion molecules. Planta Med 2004; 70:93-103.
15
16. Sedaghat R, Yaraee R, Naseri M, Naghizadeh MM. The effect of MS14 on body weight, spleen index and structures of kidney, liver, spleen, lung, lymph node and bone marrow histology in Balb/c mice. Pajouhesh dar pezeshki (Journal of Research In Medical Sciences) 2010; 34:8-12.
16
17. Hammer KDP, Hillwig ML, Solco AKS, Dixon PM. Inhibition of prostaglandin E2 production by anti-inflammatory hypericum perforatum extracts and constituents in RAW264.7 Mouse Macrophage Cells. J Agric Food Chem 2007; 55:7323–7331.
17
18. Mencherini T, Cau A, Bianco G, Della Loggia R, Aquino RP, Autore G. An extract of Apium graveolens var. dulce leaves: structure of the major constituent, apiin, and its anti-inflammatory properties. J Pharm Pharmacol 2007; 59:891-897.
18
19. Eghtedardoost M, Yaraee R, Ghazanfari T, Naseri M. The Effect of MS14 on Candidial sepsis in BALB/C mice. Iran J Infect Dis Trop Med 2009; 14:1-6.
19
20. Yaraee R, Naseri M, Eghtedardoost M, Ahmadi A. The Effect of MS14 on Th2 cytokines pattern in BALB/C mice. Immunopharmacol Immunotoxicol 2010; 32:450-453.
20
ORIGINAL_ARTICLE
Relaxatory Effect of Gamma-Aminobutyric Acid (GABA) is Mediated by Same Pathway in Diabetic and Normal Rat Mesenteric Bed vessel
Objective(s)
Diabetes related dysfunction of resistance vessels is associated with vascular occlusive diseases. Vasorelaxant agents may have a role in control of diabetic cardiovascular complications. Gamma aminobutyric acid (GABA) has demonstrated to cause vasorelaxation. The present study was designed to determine i) the vasorelaxatory effect of GABA on diabetic vessels and ii) the role of endothelium in GABAinduced vasorelaxation.
Materials and Methods
After Diabetes induction,. Mesenteric arteries of animals were perfused. Vascular beds were constrictedwith phenylephrine. GABA (1 to 50 μM) was added into the medium and perfusion pressure was then recorded.
Results
In all groups of animals, relaxant response to GABA in mesenteric bed appeared. Although diabetes induction did not change mesenteric bed response to GABA, denuded vessels showed a reduced response to GABA both in control and diabetic animals.
Conclusion
GABA can induce endothelium dependent vasorelaxation in mesenteric vessels in normal and diabetic rats.
https://ijbms.mums.ac.ir/article_4970_ff38d3d91d45d6288b163cbb013d787c.pdf
2011-01-01
94
98
10.22038/ijbms.2011.4970
Diabetes
Endothelium
GABA
Mesenteric arteries
Rat
Leila
Farsi
1
Department of Basic Sciences, Gonabad University of Medical Sciences, Gonabad, Iran
AUTHOR
Mansoor
Keshavarz
mkeshavarz@sina.tums.ac.ir
2
Department of Physiology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
Nepton
Soltani
solnep2002@yahoo.com
3
Department of Physiology, School of Medicine, Hormozgan University of Medical Sciences, Bandar Abbas, Iran
AUTHOR
1. Ozcelikay AT, Tay A, Guner S, Tasyaran V, Yildizoglu-Ari N, Dincer UD, et al. Reversal effects of L-arginine treatment on blood pressure and vascular responsiveness of streptozotocin-diabetic rats. Pharmacol Res 2000; 41:201-209.
1
2. Gammelsaeter R, Froyland M, Aragon C, Danbolt NC, Fortin D, Storm-Mathisen J, et al. Glycine, GABA and their transporters in pancreatic islets of Langerhans: evidence for a paracrine transmitter interplay. J Cell Sci 2004; 117:3749-3758.
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4. Holmgaard K, Aalkjaer C, Lambert JD, Hessellund A, Bek T. The relaxing effect of perivascular tissue on porcine retinal arterioles in vitro is mimicked by N-methyl-D-aspartate and is blocked by prostaglandin synthesis inhibition. Acta Ophthalmol 2008; 86:26-33.
4
5. Ozdem SS, Sadan G. Impairment of GABA-mediated contractions of rat isolated ileum by experimental diabetes. Pharmacology 1999; 59:165-170.
5
6. Soltani N, Keshavarz M, Sohanaki H, Zahedi Asl S, Dehpour AR. Relaxatory effect of magnesium on mesenteric vascular beds differs from normal and streptozotocin induced diabetic rats. Eur J Pharmacol 2005; 508:177-181.
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7. McGregor DD. The Effect of sympathetic nerve stimulation of vasoconstrictor responses in perfused mesenteric blood vessels of the rat. J Physiol 1965; 177:21-30.
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8. Wagner JA, Varga K, Jarai Z, Kunos G. Mesenteric vasodilation mediated by endothelial anandamide receptors. Hypertension 1999; 33: 429-434.
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10. Abe A, Kawasoe C, Kondo Y, Sato K. Enhancement of norepinephrine-induced transient contraction in aortic smooth muscle of diabetic mice. Acta Med Okayama 2003; 57:45-48.
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11. Hadi HA, Suwaidi JA. Endothelial dysfunction in diabetes mellitus. Vasc Health Risk Manag 2007; 3:853-876.
11
12. Diederich D, Skopec J, Diederich A, Dai FX. Endothelial dysfunction in mesenteric resistance arteries of diabetic rats: role of free radicals. Am J Physiol 1994; 266:H1153-1161.
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13. Touyz RM. Role of magnesium in the pathogenesis of hypertension. Mol Aspects Med 2003; 24:107-136.
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14. Erdo S, Varga B, Horvath E. Effect of local GABA administration on rat ovarian blood flow, and on progesterone and estradiol secretion. Eur J Pharmacol 1985; 111:397-400.
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15. Fergus A, Lee KS. GABAergic regulation of cerebral microvascular tone in the rat. J Cereb Blood Flow Metab 1997; 17:992-1003.
15