ORIGINAL_ARTICLE
Preventive Effect of Vitamin B6 on Developmental Toxicity of Carbamazepine in Mice
Objective(s)
Carbamazepine (CBZ) is an antiepileptic drug that is used widely for the treatment of epileptic seizures. Neural tube defects (NTDs), growth retardation, and nail hypoplasia are the most common features of teratogenic effects of this drug. The purpose of this study was to examine the effect of vitamin B6 on the developmental toxicity of CBZ on mice.
Materials and Methods
Sixty BALB/c pregnant mice were divided into four experimental and two control groups. Two experimental groups received daily intraperitoneal injection (IP) of 30 mg/kg (I) or 60 mg/kg (II) of CBZ on gestational days (GD) 6 to 15. Two other experimental groups received daily IP injection of 30 mg/kg (III) or 60 mg/kg (IV) of CBZ with 10 mg/kg/day vitamin B6 by gavage 10 days prior to gestation and on GD 6 to 15. Two control groups received normal saline or Tween 20. Dams underwent Cesarean section on GD 18 and embryos were harvested. External/macroscopic observation of fetuses was done by stereomicroscope and external examination for malformations was recorded. Data analyzed by ANOVA and X2 test using SPSS software.
Results
The mean weight and crown-rump of the fetuses in both CBZ-treated experimental groups were significantly reduced compared with those of the control groups. Various malformations were detected such as brachygnathia, eye malformations, NTDs, vertebral deformity, brachydactyly and growth retardation. Vitamin B6 treatment significantly reduced various CBZ-induced malformations.
Conclusion
This study showed that vitamin B6 has a preventive effect on the developmental toxicity of CBZ in mice that can be pursued further for clinical research.
https://ijbms.mums.ac.ir/article_4971_dc8440822cc1d6fb6bf8022d75d1d74a.pdf
2011-03-01
99
106
10.22038/ijbms.2011.4971
Carbamazepine
Congenital abnormalities
Pyridoxine
Teratology
Mice
Mohammad
Afshar
salamafshar-md@yahoo.com
1
Department of Anatomy, Birjand University of Medical Sciences, Birjand, Iran
AUTHOR
Seyed Adel
Moallem
samoallem@yahoo.com
2
Pharmaceutical Sciences Research Center, Medical Toxicology Research Center, Department of Pharmacodynamics and Toxicology, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Javad
Baharara
baharara78@gmail.com
3
Department of Biology, Azad Islamic University of Mashhad, Mashhad, Iran
AUTHOR
Toktam
Takjo
4
Department of Biology, Azad Islamic University of Mashhad, Mashhad, Iran
AUTHOR
Mohammad Jafar
Golalipour
mjgolalipour@yahoo.com
5
Gorgan Congenital Malformations Center, Golestan University of Medical Sciences, Gorgan, Iran
AUTHOR
1. Ornoy A. Neuroteratogens in man: an overview with special emphasis on the teratogenicity of antiepileptic drugs in pregnancy. Reprod Toxicol 2006; 22:214-226.
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2. Hiremath GK, Kotagal P, Bingaman W, Hovinga C, Wyllie E, Morris H, et al., Risk factors for carbamazepine elevation and toxicity following epilepsy surgery. Seizure 2005; 14:312-317.
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3. Perez Martin JM, Fernández Freire P, Labrador V, Hazen MJ. Carbamazepine induces mitotic arrest in
3
mammalian Vero cells. Mutat Res 2008; 637:124-133.
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4. Christensen HD, Rayburn WF, Parker KM, Gonzalez CL, Gold KP. Chronic prenatal exposure to carbamazepine and perinatal outcomes of C3H/He mice. Am J Obstet Gynecol 2004; 190:259-263.
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5. Matalon S, Schechtman S, Goldzweig G, Ornoy A. The teratogenic effect of carbamazepine: a meta-analysis of 1255 exposures. Reprod Toxicol 2002; 16: 9-17.
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6. Lindhout D, Hoppener RJ, Meinardi H. Teratogenicity of antiepileptic drug combinations with special emphasis on epoxidation (of carbamazepine). Epilepsia 1984; 25:77-83.
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7. Tomson T, Battino D. Teratogenic effects of antiepileptic drugs. Seizure 2008; 17:166-171.
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8. Artama M, Ritvanen A, Gissler M, Isojärvi J, Auvinen A. Congenital structural anomalies in offspring of women with epilepsy--a population-based cohort study in Finland. Int J Epidemiol 2006; 35:280-287.
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10. Afshar M, Moallem SA, Houshang Mohammadpour A, Shiravi A, Majid Jalalian S, Jafar Golalipour M. Teratogenic effects of carbamazepine on embryonic eye development in pregnant mice. Cutan Ocul Toxicol 2010; 29:10-15.
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11. Sutcliffe AG, Jones RB, Woodruff G. Eye malformations associated with treatment with carbamazepine during pregnancy. Ophthalmic Genet 1998; 19:59-62.
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12. Kannan K, Jain SK. Effect of vitamin B6 on oxygen radicals, mitochondrial membrane potential, and lipid peroxidation in H2O2-treated U937 monocytes. Free Radic Biol Med 2004; 36:423-428.
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13. Sener U, Zorlu Y, Karaguzel O, Ozdamar O, Coker I, Topbas M.Effects of common anti-epileptic drug monotherapy on serum levels of homocysteine, vitamin B12, folic acid and vitamin B6. Seizure 2006; 15:79-85.
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14. Tamura T, Aiso K, Johnston KE, Black L, Faught E. Homocysteine, folate, vitamin B-12 and vitamin B-6 in patients receiving antiepileptic drug monotherapy. Epilepsy Res 2000; 40:7-15.
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15. Perna AF, Ingrosso D, Lombardi C, Acanfora F, Satta E, Cesare CM, Violetti E, et al. Possible mechanisms of homocysteine toxicity. Kidney Int Suppl 2003: S137-140.
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16. Azarbayjani F, Danielsson BR. Pharmacologically induced embryonic dysrhythmia and episodes of hypoxia followed by reoxygenation: a common teratogenic mechanism for antiepileptic drugs. Teratology 1998; 57:117-126.
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17. Diav-Citrin O, Shechtman S, Arnon J, Ornoy A. Is carbamazepine teratogenic? A prospective controlled study of 210 pregnancies. Neurology 2001; 57:321-324.
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18. Jones KL, Lacro RV, Johnson KA, Adams J. Pattern of malformations in the children of women treated with carbamazepine during pregnancy. N Engl J Med 1989; 320:1661-1666.
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19. Vorhees CV, Acuff KD, Weisenburger WP, Minck DR. Teratogenicity of carbamazepine in rats. Teratology 1990; 41:311-317.
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20. Lumeng L, Cleary RE, Wagner R, Yu P-L, Li T-K. Adequacy of vitamin B6 supplementation during pregnancy: a prospective study. Am J Clin Nutr 1976; 29: 1376-1383.
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21. Schuster K,Bailey LB, Mahan CS. Vitamin B6 status of low-income adolescent and adult pregnant women and the condition of their infants at birth. Am J Clin Nutr 1981; 34:1731-175.
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22. Leeda M, Riyazi N, de Vries JI, Jakobs C, van Geijn HP, Dekker GA. Effects of folic acid and vitamin B6 supplementation on women with hyperhomocysteinemia and a history of preeclampsia or fetal growth restriction. Am J Obstet Gynecol 1998; 179: 135-139.
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23. Schubert J, Schmidt F, Syska E. B group vitamins and cleft lip and cleft palate. Int J Oral Maxillofac Surg 2002; 31:410-413.
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24. Piersma AH, Verhoef A, Opperhuizen A, Klaassen R, van Eijkeren J, Olling M. Embryotoxicity of carbamazepine in rat postimplantation embryo culture after in vitro exposure via three different routes. Reprod Toxicol 1998; 12:161-168.
25
25. Williams CP, Marsh CS, Hodgkins PR. Persistent fetal vasculature associated with orbital lymphangioma. J Aapos 2006; 10:285-286.
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26. Kroes HY, Reefhuis J. Natural history of homocystinuria due to cystathionine beta-synthase deficiency. Am J Hum Genet 1985; 37:1-31.
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27. Mudd SH, Skovby F, Levy HL, Pettigrew KD, Wilcken B, Pyeritz RE, et al. The natural history of homocystinuria due to cystathionine beta-synthase deficiency. Am J Hum Genet 1985; 37:1-31.
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28. Holmes LB. The teratogenicity of anticonvulsant drugs: a progress report. J Med Genet 2002; 39:245 247.
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29. Candito M, Gueant JL, Naimi M, Bongain A, Van Obberghen E. Antiepileptic drugs: a case report in a pregnancy with a neural tube defect. Pediatr Neurol. 2006; 34:323-324.
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30. Wide K, Winbladh B, Kallen B. Major malformations in infants exposed to antiepileptic drugs in ut ero, with emphasis on carbamazepine and valproic acid: a nation-wide, population-based register study. Acta Paediatr 2004; 93:174-176.
31
31. Van Rooij IA, Swinkels DW, Blom HJ, Merkus HM, Steegers-Theunissen RP. Vitamin and homocysteine status of mothers and infants and the risk of nonsyndromic orofacial clefts. Am J Obstet Gynecol 2003; 189:1155-1160.
32
32. Wong WY, Eskes TK, Kuijpers-Jagtman AM, Spauwen PH, Steegers EA, Thomas CM, et al. Nonsyndromic orofacial clefts: association with maternal hyperhomocysteinemia. Teratology 1999; 60:253-257.
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33. Fritz H, Muller D, Hess R. Comparative study of the teratogenicity of phenobarbitone, diphenylhydantoin and carbamazepine in mice. Toxicology 1976; 6:323-330.
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34. Ornoy A, Cohen E. Outcome of children born to epileptic mothers treated with carbamazepine during pregnancy. Arch Dis Child 1996; 75:517-520.
35
35. Apeland T, Froyland ES, Kristensen O, Strandjord RE, Mansoor MA. Drug-induced pertubation of the aminothiol redox-status in patients with epilepsy: improvement by B-vitamins. Epilepsy Res 2008; 82:1-6.
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36. Azarbayjani F, Danielsson BR. Embryonic arrhythmia by inhibition of HERG channels: a common hypoxiarelated teratogenic mechanism for antiepileptic drugs? Epilepsia 2002; 43:457-468.
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37. Hamelet J, Seltzer V, Petit E, Noll C, Andreau K, Delabar JM, et al. Cystathionine beta synthase deficiency induces catalase-mediated hydrogen peroxide detoxification in mice liver. Biochim Biophys Acta 2008; 1782:482-488.
38
ORIGINAL_ARTICLE
Effect of Dexamethasone on Striatal Neurotransmissions in the Rats Subjected to Parkinson’s Disease Animal Model
Objective(s)
The aim of this study was to evaluate the effects of dexamethasone on striatal dopaminergic, glutamatergic and gamma amino butyric acid (GABA) ergic neurotransmission in normal and parkinsonian rats.
Materials and Methods
Dexamethasone (0.15, 0.30, 0.60 and 0.8 mg/kg) was administered to normal or parkinsonian rats (i.p.) followed by the analysis of the striatal neurotransmitters concentrations. Additionally, the effect of dexamethasone on the damaged Substantia nigra pars compata (SNc) neurons has been investigated.
Results
Dexamethasone resulted in decreased level of striatum glutamatergic-GABAergic and enhanced dopaminergic neurotransmission in normal and parkinsonian rats. In addition, acute treatment with dexamethasone did not improve the lesion at all.
Conclusion
These findings suggest the new therapeutic mechanism of action for dexamethasone in Parkinson’s disease animal model.
https://ijbms.mums.ac.ir/article_4972_d7950b0b99d67a03051e0b76dbea0a3e.pdf
2011-03-01
107
115
10.22038/ijbms.2011.4972
Dexamethasone
Dopamine
GABA
Glutamate
Parkinson’s disease
Massoud
Amanlou
1
Department of Medicinal Chemistry, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Seyed Davar
Siadat
e-mail: d.siadat@gmail.com
2
R and D and QC consultant & Hepatitis and AIDS Department, Research and Production Complex, Pasteur Institute of Iran, Tehran, Iran
AUTHOR
Dariush
Norouzian
dnsa@pasteur.ac.ir
3
R and D and QC consultant & Hepatitis and AIDS Department, Research and Production Complex, Pasteur Institute of Iran, Tehran, Iran
AUTHOR
Mohammad Reza
Aghasadeghi
4
R and D and QC consultant & Hepatitis and AIDS Department, Research and Production Complex, Pasteur Institute of Iran, Tehran, Iran
AUTHOR
Hadi
Fathi- Moghaddam
5
Department of Physiology and Physiology Research Center, Jundishapour University of Medical Sciences, Ahvaz, Iran
AUTHOR
Mohhamad
Piryaei
6
Department of Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Mehdi
Shafiee Ardestani
shafieeardestani@gmail.com
7
Department of Medicinal Chemistry, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
LEAD_AUTHOR
1. Rowland LP. Inhibition of cyclooxygenase-2 protects motor neurons in an organotypic model of amyotrophic lateral sclerosis. Ann Neurol 2000; 48:792–795.
1
2. McGeer PL, McGeer EG. Innate immunity, local inflammation, and degenerative disease. Sci Aging Kowledge Environ 2002; 29 review 3.
2
3. McGeer PL, Schwab C, Parent A, Doudet D. Presence of reactive microglia in monkey substantia nigra years after 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine administration. Ann Neurol 2003; 54:599–604.
3
4. Smith WL, Marnett LJ, Dewitt DL.Prostaglandin and thromboxane biosynthesis. Pharmacol Ther 1991; 49:153-79.
4
5. Xie WL, Chipman GJ, Robertson DL, Erikson RL.Expression of a mitogenresponsive gene encoding prostaglandin synthase is regulated by mRNA splicing. Proc Natl Acad Sci USA 1991; 88:2692-2696.
5
6. Shaftel SS, Olschowka JA, Hurly SD. COX-3: a splice variant of cyclooxygenase-1 in mouse neural tissue and cells. Brain Res Mol Brain Res 2003; 119:153-179.
6
7. Herschman HR. Prostaglandin synthase-2. Biochem Biophys Acta 1996; 1299:153-179.
7
8. Dubois RN, Abramson SB, Crofford L, Cupta RA. Cyclooxygenase in biology and disease. FASEB J 1998; 12:1063-1073.
8
9. Li RC, Row BW, Gozal E, Fan Q, Guo SZ. Cyclooxygenase-2 and intermittent hypoxia-induced spatial defects in the rat. Am J Respir Crit Care Med 2003; 168:469-475.
9
10. Minghetti L. Cyclooxygenase-2 (COX-2) in inflammatory and degenerative brain disease. J Neuropathol Exp Neural 2004; 63:901-910.
10
11. Kurkowska-Jastrzebska I, Litwin T, Joniec I, Ciesielska A, Przybylkowski A, Czlonkowski A. Dexamethasone protects against dopaminergic neuron damage in a mouse model of Parkinson’s disease. Int Immunopharmacol 2004; 4:1307-1318.
11
12. Sánchez-Pernaute R, Ferree A, Cooper O, Yu M, Brownell L, Isacson O. Selective COX-2 inhibition prevents progressive dopamine neuron degeneration in a rat model of Parkinson's disease. J Neuroinflammation 2004; 1:6.
12
13. Mladenovic A, Perovic M, Raicevic N, Kanazir S, Rakic L, Ruzdijic S. 6- Hydroxydopamine increases the level of TNFalpha and bax mRNA in the striatum and induces apoptosis of dopaminergic neurons in hemiparkinsonian rats. Brain Res 2004; 996:237-245.
13
14. Shafiee Ardestani M, Mehrab H, Sadeghzadeh N. Effects of dexamethasone and betamethasone on rigidity in a rat model of Parkinson's disease. Indian J Pharmacol 2007; 39:235-239.
14
15. Shafiee Ardestani M, Hemmati AA, Fathi-Moghaddam H, Nazari Z. Effects of aspirin and celecoxib on rigidity in a rat model of Parkinson’s disease. Pak J Biol Sci 2007; 21:3853-3858.
15
16. Paxinos G,Watson C. The rat brain in stereotaxic coordinates. San Diego: Academic Press; 1997.
16
17. Fathi-Moghaddam H, Shafiee Ardestani, M, Saffari M, Navidpour L, Shafiee A, Rahmim A. Dopaminergic but not glutamatergic neurotransmission is increased in the striatum after selective COX-2 inhibition in normal and hemiparkinsonian rats. Basic Clin Pharmacol Toxicol 2008; 103:293-296.
17
18. Shafiee Ardestani M. Parkinson's disease, the inflammatory pathway and anti inflammatory agents: an overview. J Med Sci 2010; 10:49-58.
18
19. Kurkowska-Jastrzebska I, Litwin T, Joniec I, Ciesielska A, Przybylkowski A, Czlonkowski A, et al. Dexamethasone protects against dopaminergic neuron damage in a mouse model of Parkinson.s disease. Int Immunopharmacol 2004; 4:1307-1318.
19
20. Chopde CT, Hote MS, Mandhane SN, Muthal AV. Giucocorticoids attenuate haloperidoMnduced catalepsy through adrenal catecholamines. J Neural Transm (Gen Sect), 1995; 102:47-54.
20
ORIGINAL_ARTICLE
Effect of Aqueous-Ethanolic Extract from Rosa damascena on Guinea Pig Isolated Heart
Objective(s)
In the present study, the effects of aqueous-ethanolic extract from Rosa damascena on heart rate and contractility were examined.
Materials and Methods
Isolated guinea-pig hearts were perfused through aorta in a Langendorff mode. Heart rate (HR) and contractility were determined in the presence of four concentrations of the extract (0.1, 0.2, 0.4 and 1.0 mg %) and isoprenaline (1, 10, 100 nM and 1 μM) in comparison with baseline values in the presence and absence of propranolol (n= 10 for each group).
Results
Both isoprenaline and the extract caused increase in heart rate and contractility (P< 0.05 to P< 0.001). The percent increased in HR due to the final concentration of isoprenaline in the absence of propranolol was significantly greater than that of the extract (P< 0.01). Propranolol caused significant reduction in both HR and contractility (P< 0.05 for both) but this effect was significantly reversed by isoprenaline and the extract (P< 0.05 to P< 0.001). The percent increased in heart contractility due to the final concentration of the extract in the absence and presence of propranolol was significantly greater than that of isoprenaline (P< 0.05 for both cases). There was significant correlation between both HR and heart contractility with concentration of isoprenaline and the extract (P< 0.05 to P< 0.001).
Conclusion
In conclusion this study showed a relatively potent inotropic and chornotropic effect for Rosa damascena on isolated guinea-pig heart.
https://ijbms.mums.ac.ir/article_4974_b5786e54d5f09ee5bee192fb0848d95d.pdf
2011-03-01
116
121
10.22038/ijbms.2011.4974
Aqueous-ethanolic extract
β-adrenoceptor
Guinea-pig
Isolated heart
Rosa damascena
Mohammad Hossein
Boskabady
boskabadymh@mums.ac.ir
1
Department of Physiology and Pharmaceutical Research Centre, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Alaleh
Vatanprast
2
Department of Physiology and Pharmaceutical Research Centre, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Hydar
Parsee
3
Department of Physiology and Pharmaceutical Research Centre, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Mahbobeh
Ghasemzadeh
4
Department of Physiology and Pharmaceutical Research Centre, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
1. Libster M. Delmars integrative herb guide for nurses. Delmar 1999; 360-370.
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2. Green M. The Rose.?? Aromatic thymes 1999; 7: 11-15.
2
3. Buckle J.Clinical aromatherapy in nursing. London: Arnold, co published by singular; 1997.
3
4. Wood G, Bache F.The dispensatory of the United States of America.4th ed. Philadelphia: Griggand Elliot;1833.
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5. Ave-Sina. Law in Medicine, Interpreter; Sharafkhandy A. Tehran: Ministry of Guidance publication;1990.
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6. Zargari A. Medicinal plants.5th ed. Tehran: Tehran University publications;1992.
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7. Mahmood N, Piacenet S, Pizza C, Bruke A, Khan A, Hay A.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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8. Maleev A, Neshtev G, Stoianov S, Sheikov N.The ulcer protective and antiinflamatory effect of Bulgarian Rose oil. Eksp Med Morfol 1972; 11:55-60.
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9. Hosseini M, Rakhshandah H, Shafieenic R, Dolati K. Analgesic effect of Rosa damascena on mice. Abstract book of 16th Iranian congress of physiology and pharmacology.2003. p.167.
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10. Shafei MN, Boskabady MH. Antitussive effect of Rosa damascena in guinea pigs. Iran J Pharm Res 2003; 2:231-234.
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11. Boskabady MH, Kiani S, Rakhshandeh H. Relaxant effects of Rosa damascena on guinea pig tracheal chains. J Ethnopharmacol 2006; 106:377-382.
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12. Kwon EK, Lee DY, Lee H, Kim DO, Baek NI, Kim YE, et al. Flavonoids from the buds of Rosa damascene inhibit the activity of 3-Hydroxy-3-methylglutaryl-coenzyme a reductase and angiotensin I-converting enzyme. J Agric Food Chem 2010; 58: 882–886.
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13. Boskabady MH, Ramazani M, Tabei T. Relaxant effects of different fractions of essential oil from carum copticum on guinea pig tracheal chains. Phytother Res 2003; 17:1145-1149.
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14. Chlopicki S, Kozlovski VI, Gryglewski RJ. No-dependent vasodilation induced by nebivolol in coronary circulation is not mediated by beta-adrenoceptors or by 5 HT1A-receptors. J Physiol Pharmacol 2002; 53:615-624.
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15. Chlopicki S, Kozlovski VI, Geygewski RJ. Clonidine-induced coronary vasodilation in isolated guinea pig heart is not mediated by endothelial a2 adrenoceptors. J Physiol Pharmacol 2003; 54:511-521.
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16. Gilani AH, Janbaz KH, Aziz N, Herzig JU, Kazemi M, Choudhary MI, et al. Possible mechanism of selective inotropic activity of the n-butanolic fraction from Berberis aristata fruit. Gen Pharmacol 1999; 33:407-444.
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17. Boskabady MH, Shafei MN, Parsaee H. Effects of aqueous and macerated extracts from Nigella sativa on guinea pig isolated heart. Pharmazie 2005; 60:943-948.
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18. Boskabady MH, Shafei MN, Shakeeba A, Sangsefidi H. Effect of Crocus satirus on guinea pig isolated heart. Phytother Res 2005; 10:1002/ptr.2317
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19. Sys SU, Boels PJ, Brutsaert DL. Positive inotropic and vasodilating effects of amrinone and milrinone in isolated canine heart. J Cardiovasc Pharmacol 1987; 10:445-449.
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20. England PJ, Shahid M. Effects of forskolin on contractile response and protein phosphorylation in the isolated perfused rat heart. Biochem J 1987; 246: 687–695.
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21. Lang RM, Fellner SK, Neumann A, Bushinsky DA, Borow KM. Left ventricular contractility varies directly with blood-ionized calcium. Ann Intern Med 1988; 108: 524–529.
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22. Francis GS, Cohn J. Heart failure: mechanisms of cardiac and vascular dysfunction and the rationale for pharmacologic intervention. FASEB J 1990; 4:3068–3075.
22
ORIGINAL_ARTICLE
Effects of Maternal Lead Acetate Exposure during Lactation on Postnatal Development of Testis in Offspring Wistar Rats
Objective(s)
During recent years, there has been an increasing interest in contribution of environmental pollutants as heavy metals to human male infertility. Present study was aimed to investigate the effects of maternal lead acetate exposure during lactation on postnatal development of testis in offspring rats.
Materials and Methods
A total of 60 female rats randomly divided into four equal groups; control and three treatment groups received 20, 100 and 300 mg/kg/day lead acetate via drinking water from day 2 to day 21 of lactation. At 7, 14, 21, 28, 60, 90 and 120 days after birth, the testis weight and volume of offspring were measured and their epididymal semen analyzed. Following tissue processing, 5 μm sections were stained with haematoxylineosin and evaluated with quantitative techniques. Testicular parameters in different groups were compared by one-way ANOVA.
Results
Testis weight and volume of offspring decreased significantly in a dose-related manner in moderate (P< 0.05) and high (P< 0.01) doses groups. Dose-dependent significant reductions were seen in seminiferous tubules diameter and germinal epithelium height during neonatal, prepubertal and postpubertal periods in moderate (P< 0.05) and high (P< 0.01) doses groups until 90 and 120 days after birth, respectively. Significant decreases were observed in mean sperm density of offspring at puberty in moderate and high doses groups until 90 and 120 days after birth, respectively. Testosterone levels decreased significantly in a dose-related manner at puberty in moderate and high doses groups.
Conclusion
Present study showed maternal lead acetate exposure during lactation caused dose-related and long-term alterations of testicular parameters in offspring rats.
https://ijbms.mums.ac.ir/article_4976_4ec4296eeece62bc9bf4d76da4fdbfa3.pdf
2011-03-01
122
131
10.22038/ijbms.2011.4976
Lead acetate
Male Infertility
Postnatal development
Testis
Mehran
Dorostghoal
mdorostghoal@yahoo.com
1
Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahwaz, Ahwaz, Iran
LEAD_AUTHOR
Abdolrahaman
Dezfoolian
2
Department of Anatomical Sciences, Faculty of Medicine, Jondishapour Medical Sciences University of Ahwaz, Ahwaz, Iran
AUTHOR
Foroogh
Sorooshnia
3
Department of Biology, Faculty of Sciences, Shahid Chamran University of Ahwaz, Ahwaz, Iran
AUTHOR
1. Adamopoulos DA, Pappa A, Nicopoulou S, Andreou E, Karamertzanis M, Michopoulos J, et al. Seminal volume and total sperm number trends in men attending subfertility clinics in the greater Athens area during the period 1977-1993. Hum Reprod 1996; 11:1936-1941.
1
2. Auger J, Kunstmann JM, Czyglik F, Jouannet P. Decline in semen quality among fertile men in Paris during the past 20 years. N Engl J Med 1995; 332:281-285.
2
3. Becker S, Berhane K. Ameta-analysis of 61 sperm count studies revisited. Fertil Steril 1997; 67:1103-1108.
3
4. Carlsen E, Giwercman A, Keiding N, Skakkebaek NE. Evidence for decreasing quality of semen during the past 50 years. Br Med J 1992; 305: 609-613.
4
5. Bonde JE. The risk of male subfertility attributable to the welding of metals. Int J Androl 1993; 16:1-23.
5
6. Spinelli A, Figa-Talamanca I, Osborn I. Time to pregnancy and occupation in a group of Italian women. Int J Epidemiol 1997; 26: 601-609.
6
7. Benoff S, Jacob A, Hurley IR. Male infertility and environmental exposure to lead and cadmium. Hum Reprod Update 2000; 6:107-121.
7
8. Benoff S, Centola GM, Millan C, Napolitano B, Marmar JL, Hurley IR. Increased seminal plasma lead levels adversely affect the fertility potential of sperm in IVF. Hum Reprod 2003; 18: 374-383.
8
9. Wong WY, Thomas CMG, Merkus JMWM, Zielhuis GA, Steegers-Theunissen RPM. Male factor subfertility: possible causes and the impact of nutritional factor. Fertil Steril 2000; 73:435-442.
9
10. Cullen M, R, Kayne RD, Robins JM. Endocrine and reproductive dysfunction in men associated with occupational inorganic lead intoxication. Arch Environ Health 1984; 39:431-440.
10
11. Foster WG, McMahon A, Younglai EV, Hughes EG, Rice EC. Reproductive endocrine effects of chronic lead exposure in the male cynomolgus monkey. Reprod Toxicol 1993; 7:203-209.
11
12. Singh A, Cullen C, Dykeman A, Rice D, Foster W. Chronic lead exposure induces ultrastructural alterations in the monkey testis. J Submicrosc Cytol Pathol 1993; 25:479-486.
12
13. Sokol RZ. Hormonal effects of lead acetate in the male rat: mechanism of action. Biol Reprod 1987; 37:1135-1138.
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14. McGivern RF, Sokol RZ, Berman NG. Prenatal lead exposure in the rat during the third week of gestation: Long-term behavioral, physiological, and anatomical effects associated with reproduction. Toxicol Appl Pharmacol 1991; 110:206-215.
14
15. Bogden JD, Gertner SB, Christakos S, Kemp FW, Yang Z, Katz SR, et al. Dietary calcium modifies concentrations of lead and other metals and renal calbindin in rats. J Nutr 1992; 122:1351-1360.
15
16. Corpas I, Castillo M, Marquina D, Benito MJ. Lead intoxication in gestational and lactation periods alters the development of male reproductive organs.Ecotoxicol Environ Saf 2002; 53:259-266.
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21. Sprando RL. Perfusion of the rat testis through the heart using heparin. In: Russell LD, Ettlin RA, Sinha HAP, Clegg ED, editors. Histological and Histopathological Evaluation of the Testis. Clearwater:Cache River Press;1990.p.277-280.
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23. Seed J, Chapin RE, Clegg ED, Dostal LA, Foote RH, Hurtt ME, et al. Methods for assessing sperm motility, morphology and counts in the rat, rabbit and dog: a consensus report. ILSI Risk Science Institute Expert Working Group on Sperm Evaluation. Reprod Toxicol 1996; 10:237–244.
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24. Narayana K, Prashanthi N, Nayanatara A, Kumar HH, Abhilash K, Bairy KL. Effects of methyl parathion (o,odimethyl o-4-nitrophenyl phosphorothioate) on rat sperm morphology and sperm count, but not fertility, are associated with decreased ascorbic acid level in the testis. Mutat Res 2005; 588:28-34.
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25. Gagnon C. The roles of environmental toxins in unexplained male infertility. Sem Reprod Endocrinol 1988; 6: 369-376.
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26. Barry PSI. A comparison of concentration of lead in human tissues. Br J Ind Med 1975; 32: 19-136.
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29. Graça A, Ramalho-Santos J, Pereira ML. Effect of lead chloride on spermatogenesis and sperm parameters in mice. Asian J Androl 2004; 6:237–241.
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30. Allouche L, Hamadouche M, Touabti A. Chronic effects of low lead levels on sperm quality, gonadotropins and testosterone in albino rats. Exp Toxicol Pathol 2009; 61:503-510.
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31. Al-Omar MA, Abbas AK, Al-Obaidy SA. Combined effect of exposure to lead and chlordane on the testicular tissues of Swiss mice. Toxicol lett 2000; 10:1-8.
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32. Coogan TP, Shiraishi N, Waalkes MP. Apparent quiescence of the metallothionein gene in the rat ventral prostate: Association with cadmium-induced prostate tumours in rats. Environ Health Perspect 1994; 102: 137-139.
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34. Moorman WJ, Skaggs SR, Clark JC, Turner TW, Sharpnack DD, Murrell JA, et al. Male reproductive effects of lead, including species extrapolation for the rabbit model. Reprod Toxicol 1998; 12:333-346.
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35. Sokol RZ. Reversibility of the toxic effect of lead on the male reproductiv eaxis. Reprod Toxicol 1989; 3:175- 180.
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37. Camoratto AM. Inhibition of rat pituitary growth hormone release by subclinical levels of lead. Toxicologists 1990; 10:641.
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38. Assennato G, Paci C, Baser ME, Molinini R, Candela, RG, Altamura BM, et al. Sperm count suppression without endocrine dysfunction in lead-exposed men. Arch Environ Health 1987; 42:124-127.
38
39. Murthy RC. Lead induced ultrastructural changes in the testis of rats. Exp Pathol 1991; 42:95-100.
39
ORIGINAL_ARTICLE
Biofilm Formation and Detection of IcaAB Genes in Clinical Isolates of Methicillin Resistant Staphylococcus aureus
Objective(s)
Methicillin-resistant Staphylococcus aureus (MRSA) is an important cause of nosocomial and community
infections. Biofilm formation, mediated by a polysaccharide intercellular adhesin (PIA) and encoded by the ica operon, is considered to be an important virulence factor in both S. epidermidis and S. aureus. However, the clinical impact of the ica locus and PIA production is less well described in S. aureus. We studied biofilm formation in clinical isolates of MRSA in relation to the presence of the ica operon.
Materials and Methods
Forty five MRSA were studied for biofilm formation by colony morphology on Congo red agar (CRA) and the microtitre plate assay (MtP). Presence of the ica genes was detected by PCR and specific primers.
Results
The results showed that 53.3% of the isolates had the potential to form biofilm by colony morphology of which, 75% carried the ica operon. Weak biofilm production was observed in the MtP assay by 57.8%, of which 53.8% harbored the ica operon. However, about 70% of biofilm non-producers also carried the ica operon.
Conclusion
Overall, there was no agreement between the icaAB gene carriage and biofilm phenotype by either of the two phenotypic methods. However, 91% of biofilm formers on CRA also produced biofilm in the MtP assay.
https://ijbms.mums.ac.ir/article_4978_fe9ec81b22536a4cd4c65323c450324e.pdf
2011-03-01
132
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10.22038/ijbms.2011.4978
biofilm formation
IcaAB
MRSA
Staphylococcus aureus
Fereshteh
Eftekhar
f-eftekhar@sbu.ac.ir
1
Microbiology Department, Faculty of Biological Sciences, Shahid Beheshti University, G.C., Evin, Tehran, Iran
LEAD_AUTHOR
Taraneh
Dadaei
2
Microbiology Department, Faculty of Biological Sciences, Shahid Beheshti University, G.C., Evin, Tehran, Iran
AUTHOR
1. Tiemersma EW, Bronzwear LAM, Lyytikainen O, Degener JE, Schrijnemakers P Bruinsma N, et al. Methicillin resistant Staphylococcus aureus in Europe, 1999-2002. Emerg Infect Dis 2004; 10:1627-134.
1
2. Cramton SE, Gerke C, Schnell NF, Nichols WW, Gotz F. The intercellular adhesin locus (ica) is present in Staphylococcus aureus and is required for biofilm formation. Infect Immun 1999; 67:5427-5433.
2
3. Gotz F. Staphylococcus and biofilms. Mol Microbiol 2002; 43:1367-1378.
3
4. Heilmann C, Schweitzer O, Gerke C, Vanittanakom N, Mack D, Götz F. Molecular basis of intercellular adhesion in the biofilm-forming Staphylococcus epidermidis. Mol Microbiol 1996; 20:1083-1091.
4
5. Arciola CR, Baldassarri L, Montanaro L. Presence of icaA and icaD genes and slime production in a collection of staphylococcal strains from catheter-associated infections. J Clin Microbiol 2001; 39:2151-2156.
5
6. Fowler VG Jr, Fey PD, Reller LB, Chamis AL, Corey GR, Rupp ME. The intercellular adhesin locus ica is present in clinical isolates of Staphylococcus aureus from bacteremic patients with infected and uninfected prosthetic joints. Med Microbiol Immunol 2001; 189:127-131.
6
7. Rohde H, Knobloch JK, Horstkotte MA, Mack D. Correlation of biofilm expression types of Staphylococcus epidermidis with polysaccharide intercellular adhesin synthesis: evidence for involvement of icaADBC genotypeindependent factors. Med Microbiol Immun 2001; 190:105-112.
7
8. Ziebuhr W, Krimmer V, Rachid S, Lössner I, Götz F, Hacker J. A novel mechanism of phase variation of virulence in Staphylococcus epidermidis: evidence for control of the polysaccharide intercellular adhesion synthesis by alternating insertion and excision of the insertion sequence element IS256. Mol Microbiol 1999; 32:345-356.
8
9. McKenney D, Pouliot K L, Wang Y, Murthy V, Ulrich M, Doring G, Lee JC, Goldmann DA, Pier GB. Broadly protective vaccine for Staphylococcus aureus based on an in vivo-expressed antigen. Science 1999; 284:1523- 1527.
9
10. Beenken KE, Blevins JS, Smeltzer MS. Mutation of sarA in Staphylococcus aureus limits biofilm formation. Infect Immun 2003; 71:4206-4211.
10
11. National Committee for Clinical Laboratory Standards (NCCLS). Performance standards for antimicrobial disk susceptibility test. 6th ed. Approved Standard. M100-A6. Wayne, PA, 1997.
11
12. National Committee for Clinical Laboratory Standard (NCCLS). Performance standards for antimicrobial susceptibility testing. 9th ed. International Supplement. M100-S9. Wayne, PA, 1999.
12
13. Handke LD, Conlon KM, Slater SR, Elbaruni S, Fitzpatrick F, Humphreys H, et al. Genetic and phenotypic analysis of biofilm phenotypic variation in multiple Staphylococcus epidermidis strains. J Med Microbiol 2004; 53:367-374.
13
14. Aricola CR, Compoccia D, Baldassarri L, Donati ME, Pirini V, Gamberini S, et al. Detection of biofilm formation in Staphylococcus epidermidis from implant infections. Comparison of a PCR method that recognizes the presence of ica genes with two classic phenotypic methods. J Biomed Mater Res 2005; 76:425-430.
14
15. Eftekhar F, Speert DP. Biofilm formation by persistent and non-persistent isolates of Staphylococcus epidermidis from a neonatal intensive care unit. J Hosp Infect 2009; 71:112-116.
15
16. Pérez-Roth E, Claverie-Martín F, Villar J, Méndez-Álvarez S. Multiplex PCR for simultaneous identification of Staphylococcus aureus and detection of methicillin and mupirocin resistance. J Clin Microbiol 2001; 39:4037-4041.
16
17. Martin-Lopez JV, Perez-Roth E, Claverie-Martin F, Diez-Gil O, Batista N, MoralesM, et al. Detection of Staphylococcus aureus clinical isolates harboring the ica gene cluster needed for biofilm establishment. J Clin Microbiol 2002; 40:1569-1570.
17
18. Grinholc M, Wegrzyn G, Kurlenda J. Evaluation of biofilm production and prevalence of the icaD gene in methicillin-resistant and methicillin-susceptible Staphylococcus aureus strains isolated from patients with nosocomialinfections and carriers. FEMS Immunol Med Microbiol 2007; 50:375-379.
18
19. Yazdani R, Oshaghi M, Havayi A, Pishva E, Salehi R, Sadeghizadeh M, et al. Detection of icaAD gene and biofilm formation in Staphylococcus aureus isolates from wound infections. Iran J Publ Health 2006; 35:25-28.
19
20. Fitzpatrick F, Humphreys H O’Gara JP. Evidence for icaADBC independent biofilm development mechanism in methicillin-resistant Staphylococcus aureus clinical isolates. J Clin Microbiol 2005; 43:1973-1976.
20
21. Rachid S, Ohlsen K, Wallner U, Hacker J, Hecker M, Ziebuhr W. Alternative transcription factor B is involved in regulation of biofilm expression in a Staphylococcus aureus mucosal isolate. J Bacteriol 2000; 182:6824-6826.
21
22. Cramton SE, Ulrich M, Götz F, Döring G. Anaerobic conditions induce expression of polysaccharide intercellular adhesin in Staphylococcus aureus and Staphylococcus epidermidis. Infect Immun 2001; 69:4079-4085.
22
23. O’Neill E, Pozzi C, Houston P, Smyth D, Humphreys H, Robinson DA, et al. Association between methicillin susceptibility and biofilm regulation in Staphylococcus aureus isolates from device-related infections. J Clin Microbiol 2007; 45:1379-1388.
23
24. Eftekhar F, Mirmohamadi Z. Biofilm formation by clinical and normal skin isolates of Staphylococcus epidermidis. Int J Med Med Sci 2009; 10:438-441.
24
ORIGINAL_ARTICLE
Prognostic Significance of MMP2 and MMP9 Functional Promoter Single Nucleotide Polymorphisms in Head and Neck Squamous Cell Carcinoma
Objective(s)
Matrix metalloproteinases comprise a family of enzyme that is able to degrade components of extra cellular matrix. There are single nucleotide polymorphisms in the promoter regions of several genes with ability to influence cancer susceptibility. The aim of this study was to analyses association between MMP2 and MMP9 promoter polymorphisms and head and neck squamous cell carcinoma occurrence and progression.
Materials and Methods
A case- control study was performed including 80 head and neck squamous cell carcinoma patients and healthy controls for MMP2 and 86 head and neck squamous cell carcinoma patients and 72 healthy controls for MMP9. Blood samples were genotyped for MMP2 and MMP9 using polymerization chain reaction– restriction fragment length polymorphism method (PCR-RFLP). Statistical analysis was performed using SPSS 12.0 software.
Results
Our results showed that distribution of MMP2 genotype between controls and patients was significantly different (χ2= 10.3, P= 0.005). Comparison between CC genotype in HNSCC patients and controls showed that C allele modified the risk of HNSCC progression (OR= 2.6, 95% CI, 1.0046–6.729). The MMP9 genotype distribution among HNSCC patients was significantly different (χ2= 14.56, P= 0.0007). The frequency of TT genotype in HNSCC patients was different from healthy controls and was more common genotype in HNSCC cases (OR= 2.18, 95% CI, 0.7052–6.7854).
Conclusion
Our results suggested an association of the MMP2 and MMP9 SNP with the development of HNSCC. Also, our results showed that MMP, MMP9 genotypes and smoking were related to HNSCC progression.
https://ijbms.mums.ac.ir/article_4979_21d961d3bcd22cf393f2c24b865533eb.pdf
2011-03-01
137
144
10.22038/ijbms.2011.4979
Extra cellular matrix
Head and neck squamous cell carcinoma
Matrix metalloproteinase
Samaneh
Hajihoseini
shajihoseiny@yahoo.com
1
HIV and Hepatitis Research Center, Faculty of Laboratorial Sciences, Gerash, Fars, Iran
LEAD_AUTHOR
Mirza Khalil
Bahmani
2
HIV and Hepatitis Research Center, Faculty of Laboratorial Sciences, Gerash, Fars, Iran
AUTHOR
Ayyoob
Khosravi
3
Golestan University of Medical Sciences, Gorgan, Golestan, Iran
AUTHOR
Eslam
Ghezelsofla
mohsen914@yahoo.com
4
HIV and Hepatitis Research Center, Faculty of Laboratorial Sciences, Gerash, Fars, Iran
AUTHOR
Abbas
Ghaderi
5
Cancer Research Institute, Shiraz University of Medical Sciences, Shiraz, Fars, Iran
AUTHOR
1. Werb Z. ECM and cell surface proteolysis: regulating cellular ecology. Cell 1997; 91:439–442.
1
2. Fang S, Jin X, Wang R, Li Y, Guo W, Wang N, et al. Polymorphism in the MMP-1 and MMP-3 promoter an non- small cell lung carcinoma in the north of China. Carcinogenesis 2005; 26:481-486.
2
3. Zhou G., Zhai Y, Qui W, Dong X, Peng Y, He F. Functional polymorphisms and haplotypes in the promoter of the MMP2 gene are associated with risk of nasopharyngeal carcinoma. Hum Mut 2007; 28:1091-1097.
3
4. Egeblad M, Werb Z.New functions for the matrix metalloproteinases in cancer progression. Nat Rev Cancer 2002; 2: 161-174.
4
5. Ghilardi G, Bionidi ML, Caputo M, Leviti S, Demonti M, Guagnellini E, et al. A single nucleotide polymorphism in the matrix metalloproteinase-3 promoter enhances breast cancer susceptibility. Clin Cancer Res 2002; 11:121-125.
5
6. Folgueras AR, Pendas AM, Sanchez LM, Lopez-Otin C. Matrix metalloproteinases in cancer: from new functions to improved inhabitation strategies. Int J Dev Biol 2004; 48:411-424.
6
7. Tower GB, Coon CC, Benbow U, Brinckerhoff CE. Erk 1/2 diffrentially regulates the expression from the IG/2G single nucleotide polymorphism in the MMP1 promoter in melanoma cell. Biochim Biophys Acta 2002; 1586:265-274.
7
8. Miao X, Yu C, Tan W, Xiong P, Liang G, Lu W, et al. A functional polymorphism in the matrix metalloproteinase -2 gene promoter (-1306C/T) is associated with risk of development but not metastasis of gastric cardia adenocarcinoma. Cancer Res 2003; 63: 3987-3990.
8
9. Yu C, Zhou Y, Miao X, Xiong P, Tan W, Lin D. Functional haplotypes in the promoter of matrix metalloproteinase -2 predicts risk of the occurrence and metastasis of esophageal cancer. Cancer Res 2004; 64:7622-7628.
9
10. Huhtala P, Chow LT, Tryggvason K. Structure of the human type IV collagenase gene. J Biol Chem 1990; 265:11077-11082.
10
11. Price SJ, Greves DR, Watkins H. Identification of novel functional genetic varients in the human matrix metalloproteinase- 2 gene. Role of Sp1 in allele specific transcriptional regulation. J Biol Chem 2001; 276:7549-7558.
11
12. Vasku A, Goldbergova M, Vacha J.A haplotype constituted of four MMP2 promoter polymorphisms (-1575G/A, -1306C/T, -790T/G and -735C/T) is associated with coronary triple- vessel disease. Matrix Biol 2004; 22:585-591.
12
13. Joos L, He JQ, Shpherdson MB, Sandfors AJ.The role of matrix metalloproteinase polymorphisms in the rate of decline in lung function. Hum Mol Genet 2002; 11:569-576.
13
14. Azzam HS, Arand G, Lippman ME, Thomson EW. Association of MMP2 activation potential with metastasic progression in human breast cancer cell lines independent of MMP2 production. J Natl Cancer Inst 2000; 85:1758-1764.
14
15. Puokolainen H, Paakko P, Turpeenniemi – Hujanen T. Expression of matrix metalloproteinase -9 in head and neck squamous cell carcinoma: a potential marker for prognosis. Clin Cancer Res 2004; 10:3110-3116.
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16. Parkin DM, Laara E, Muir CS. Estimates of the worldwide frequency of sixteen major cancers in 1980. Int J Cancer 1988; 41:184–197.
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17. Herve' J, LeBoeuf MD. Chemotherapy for head and neck cancer. Otolaryngology 1998.
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18. Chambers AF, Matrisian LA. Changing views on the role of matrix metalloproteinases in metastasis. J Natl Cancer Inst 1997; 89: 1260-1270.
18
19. Kripple P, Langsenlehner U, Renner W, Yazdani- Biuki B, Koppel H, Leithner AC, et al. The 5A/6A polymorphism of matrix metalloproteinase-3 gene promoter and breast cancer. Clin Cancer Res 2004; 10:3518-3520.
19
20. Motovali-Bashi M, Hojati Z, Hajihoseini S.The role of matrix metalloproteinase-3 functional 5A/6A promoter polymorphism in tumor progression and metastasis of breast cancer. IJB 2008; 6: 45-49.
20
21. Motovali-Bashi M, Hojati Z, Kouhkan F. Genetic variation in MMP1 promoter region and breast cancer susceptibility. J Sci IRIran 2008; 19:9-14.
21
22. Kouhkan F, Motovali-Bashi M, Hojati Z. The influence of interstitial Collagenase-1 genotype polymorphism on colorectal cancer risk in Iranian population. Cancer Invest 2008; 26:836-842.
22
23. Yu C, Zhou Y, Miao X, Xiong P, Tan W, Lin D. Functional haplotypes in the promoter of matrix metalloproteinase -2 predicts risk of the occurrence and metastasis of esophageal cancer. Cancer Res 2004; 64:7622-7628.
23
24. Lu J, Chua HH, Chen SY, Chen JY, Tsai CH. Regulation of matrix metalloproteinase -1 by Epstein – Barr virus proteins. Cancer Res 2003; 63:256-262.
24
25. Yoshizaki T, Sato H, Furukawa M. Recent advances in the regulation of matrix metalloproteinase -2 activation:from basic research to clinical implication. Oncol Rep 2002; 9:607-611.
25
26. Ye S, Eriksson P, Hamsten A, Kurkinen M, E-Humphries S, M- Henney A. Progression of coronary atherosclerosis is associated with a common genetic variation of the human stromelysin-1 promoter which results in reduced gene expression. Biol Chem 1996; 271:13055-13060.
26
27. Lahman C, Beremann J, Harrison G, Young AR. Matrix metalloproteinase -1 and skin aging in smoker. Lancet 2001; 357:935-936.
27
28. Miyajima Y, Nakano R, Morimatsu M. Analysis of expression of matrix metalloproteinases-2 and-9 in hypopharyngeal squamous cellcarcinoma by in situ hybridization.Ann Otol Rhinol Laryngol 1995; 104:678–684.
28
29. Franchi A, Santucci M, Masini E, Sardi I, Paglierani M, Gallo O. Expression of matrix metalloproteinase 1, matrix metalloproteinase 2, and matrix metalloproteinase 9 in carcinoma of the head and neck. Cancer (Phila.) 2002; 95:1902–1910.
29
30. Scorilas A, Karameris A, Arnogiannaki N, Ardavanis A, Bassilopoulos P, Trangas T, et al. Overexpression of matrix-metalloproteinase-9 in human breast cancer: a potential favourableindicator in node-negative patients. Br J Cancer 2001; 84:1488–1496.
30
ORIGINAL_ARTICLE
The Effect of Sun Radiation on the Course of Cutaneous Leishmaniasis in BALB/c Mice
Objective(s)
Studies have described immunomedulatory effects of sun exposure and ultraviolet radiation on infectious and neoplastic diseases. Here the effect of exposure to low potency radiation of sun on the course of leishmaniasis in mice was studied.
Materials and Methods
Fifteen BALB/c mice were exposed to suberythemogenic doses of sun (mean 180 mJ/cm2/day of UVB) 2 months before and 4 months after Leishmania major inoculation to food pad. Control group was kept in the sun protected environment. From 2nd to 17th week after inoculation, size of the lesion was recorded in each group weekly and at last week the parasite burden in spleen was detected. Results were compared between two groups.
Results
Seven mice from case group and 9 mice from control group survived up to last week. The mean lesion size was 0.90±0.59 cm in exposed and 4.01±3.59 cm in unexposed mice (P= 0.037). Parasite burden in spleen of case and control groups were 5.5±4.61 and 106.94±279.76 respectively (P= 0.006).
Conclusion
Chronic exposure of BALB/c mice to suberythemogenic doses of sun suppressed skin lesion and decreased the extension of L. major to spleen.
https://ijbms.mums.ac.ir/article_4980_ee8a374198a4a022ddb8dbf529396b62.pdf
2011-03-01
145
150
10.22038/ijbms.2011.4980
Immunity
Leishmaniasis
Sunlight
Fateme
Hoseinipoor
1
Department of Dermatology, Emamreza Hospital, Mashhad, Iran
AUTHOR
Mahnaz
Banihashemi
2
Department of Dermatology, Gaem Hospital, Mashhad, Iran
AUTHOR
Mohammad Reza
Jaafari
3
Biotechnology Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Zari
Javidi
4
Department of Dermatology, Emamreza Hospital, Mashhad, Iran
AUTHOR
Amir Abas
Azarian
5
Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Vahid
Mashayekhi Goyonlo
mashayekhiv@mums.ac.ir
6
Department of Dermatology, Emamreza Hospital, Mashhad, Iran
LEAD_AUTHOR
1. Ardehali SD, Rezaee HR, Nadim AH. Leishmaniasis and Leishmania parasite. Tehran-Iran: Tehran university publication center; 1985.
1
2. Kemp M, Hey AS, Kurtzhals JA, Christensen CB, Gaafar A, Mustafa MD, et al. Dichotomi of the T cell responseto Leishmania antigens. I.Th1-like response to Leishmania major promastigote antigens in individuals recovered from cutaneousleishmaniasis. Clin Exp Immunol 1994; 96:410–415.
2
3. Lopez, FV, Hay RJ. Parasitic worms and protozoa. In: Burns T, Breathnatch S, Cox N, Griffiths C. Rook’s Text book of Dermatology .8th ed.Oxford: Blackwell Science; 2010.p. 33-38.
3
4. Ghosn S, Kurban A. Leishmaniasis and other protozoan in infections. In: Wolff K, Gold Smith L, Katz S, Gilchrest BA, Paller AS, Leffell DJ. Fitzpatrick's Dermatology in General Medicine. 7th ed. New York: Mc Graw Hill; 2008.p. 2001-2010.
4
5. Hawk JLM, Young AR, Ferguson J. Cutaneous Photobiology. In: Burns T, Breathnatch S, Cox N, Griffiths C. Rook’s Text book of Dermatology. 8th ed.Oxford: Mc Graw Hill; 2010.p.1-29.
5
6. Musa AM, Khalil EA, Raheem MA, Zijlstra EE, Ibrahim ME, Elhassan IM, et al. The natural history of Sudanese post-kala-azar dermal leishmaniasis: clinical, immunological and prognostic features. Ann Trop Med Parasitol 2002; 96:765–772.
6
7. Ismail A, Khalil EA, Musa AM, El Hassan IM, Ibrahim ME, Theander TG, et al. The pathogenesis of post kalaazar dermal leishmaniasis from the field to the molecule: does ultraviolet light (UVB) radiation play a role? Med Hypotheses 2006; 66:993–999.
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8. Khaskhely NM, Maruno M, Uezato H, Takamiyagi A, Ramzi ST, Al-Kasem KM, et al. Low-dose UVB contributes to host resistance against Leishmania amazonensis infection in mice through induction of gamma interferon and tumor necrosis factor alpha cytokines. Clin Diagn Lab Immunol 2002; 9:677-686.
8
9. Jaafari MR, Bavarsad N, Fazly Bazzaz A, Samiei A, Soroush D, Ghorbani S, et al. The effect of topical liposomes containing paromomycin sulfate (PM) in the course of Leishmania major infection in susceptible BALB/c mice. Antimicrob Agents Chemother 2009; 53:2259-2265.
9
10. Jaafari MR, Ghafarian A, Farrokh-Gisour A, Samiei A, Kheiri MT, Mahboudi F. Immune response and protection assay of recombinant major surface glycoprotein of Leishmania (rgp63) reconstituted with liposomes in BALB/c mice. Vaccine 2006; 24: 708-5717.
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11. Brown EL, Rivas JM, Ullrich SE, Young CR,Norris SJ, Kripke ML. Modulation of immunity to Borrelia burgdorferi by ultraviolet irradiation: differential effect on Th1 and Th2 immune responses. Eur J Immunol 1995; 25:3017-3022.
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13. Howie S, Norval M, Maingay J. Exposure to low-dose ultraviolet radiation suppresses delayed- Type hypersensitivity to herpes simplex virus in mice. J Invest Dermatol 1986; 86: 125-128.
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14. Jeevan A, Kripke ML. Effect of a single exposure to ultraviolet radiation on Mycobacterium bovis bacillus Calmette- Guerin infection in mice. J Immunol 1989; 143:2837-2843.
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15. Jeevan A, Gilliam K, Heard H, Kripke ML. Effects of ultraviolet radiation on the pathogenestis of Mycobacterium lepraemurin in mice. Exp Dermatol 1992; 1:152-160.
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16. Noonan FP, Alewis FA. UVB- induced immune suppression and infection with Schistosoma mansoni. Photochem Photobiol 1995; 61:99-105.
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17. Garssen J, Vandebriel RJ, De Gruijl FR, Wolvers DA, Van Dijk M, Fluitman A.UVB exposure- induced systemic modulation of Th1-and Th2-mediated immune responses. Immunology 1999; 97:506-514.
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18. Reiner SL, Locksley RM. The regulation of immunity to Leishrmania major. Annu Rev Immunol 1995; 13:151-177.
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19. Abbas AK, Murphy KM, Sher A. Functional diversity of helper T lymphocytes. Nature 1996; 383:787-793.
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20. Louis J, Himmelrich H, Parra-Lopez C, Tacchini-Cottier F, Launois P.Regulation of protective immunity against Leishmania major in mice. Curr Opin Immunol 1998; 10:459-464.
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21. Schade N, Esser C, Krutmann J. Ultraviolet B radiation-induced immunosuppression: molecular mechanisms and cellular alterations. Photochem Photobiol Sci 2005; 4:699-708.
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22. Schwarz T. Mechanisms of UV-induced immunosuppression. Keio J Med 2005; 54:165–171.
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23. Sleijffers A, Garssen J, Vos JG, Loveren H. Ultraviolet light and resistance to infectious diseases. J Immunotoxicol 2004; 1:3-14.
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24. Narbutt J, Lesiak A, Sysa-Jedrzejowska A, Wozniacka A, Cierniewska-Cieslak A, Boncela J,et al. Repeated low-dose ultraviolet (UV) B exposures of humans induce limited photoprotection against the immune effects of erythemal UVB radiation. Br J Dermatol 2007; 156: 539-547.
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25. McLoone P, Norval M. Adaptation to the UV-induced suppression of phagocytic activity in murine peritoneal macrophages following chronic exposure to solar simulated radiation. Photochem Photobiol Sci 2005; 4:792-797.
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26. Giannini MS. Suppression of pathogenesis in cutaneous leishmaniasis by UV irradiation. Infect Immun 1986; 51:838-843.
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31
ORIGINAL_ARTICLE
The Effects of Achillea wilhelmsii Extract on Rat’s Gastric Motility at Basal and Vagal Stimulated Conditions
Objective(s)
Achillea genius is widely used in traditional medicine for gastrointestinal disorders. The aim of this study was to investigate the effects of aqueous-ethanol extract of Achillea wilhelmsii on rat’s gastric motility in basal and vagal stimulated conditions.
Materials and Methods
Twenty four Wistar rats were randomly divided into two groups: control and test. The extract was prepared by maceration which was used to prepare three 0.5 ml samples of three doses (0.5, 1 and 2 mg/kg) in the test group. The same volume of saline was used in the control group. Gastric motility was measured by inserting a small balloon in the stomach which was connected to a pressure transducer. The data were recorded for 25 min duration after each dose and these data were analyzed for 3 intermittent five min intervals (t1= 0-5, t2= 10-15 and t3= 20-25 min).
Results
The extract at basal condition decreased intragastric pressure (IGP) by 1 mg/kg dose in the t3 and 2 mg/kg in the t2 and t3 intervals. The extract at vagal stimulated condition decreased IGP by 1 and 2 mg/kg doses in the t2 and t3 intervals. The extract reduced contraction amplitude at basal condition by 2 mg/kg dose in the t2 and t3 intervals. At vagal stimulated condition contraction amplitude was reduced by 1 mg/kg dose in the t2 and t3 by 2 mg/kg in all three intervals. The extract showed no effect on frequency of gastric contraction in either basal or vagal stimulated conditions.
Conclusion
The extract showed an inhibitory effect on gastric motility in both basal and vagal stimulated condition. This inhibitory effect may be exerted by an antagonistic effect on acetylcholine dependent calcium influx or release of calcium from intracellular storage in gastric smooth muscle.
https://ijbms.mums.ac.ir/article_4981_d8265a7f4a5bd33ab1010bedb1485222.pdf
2011-03-01
151
157
10.22038/ijbms.2011.4981
Achillea wilhelmsii
Gastrointestinal Motility
Vagus Nerves
Saeed
Niazmand
niazmands@mums.ac.ir
1
Department of Physiology and Cardiovascular Research Center, Medical School, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Esmat
Khoshnood
2
Department of Biology, Sciences School, Azad University of Mashhad, Mashhad, Iran
AUTHOR
1. Kasper DL. Harrison's principels of internal medicine. 16th ed. New york:McGraw- Hill medical publishing division; 2005.
1
2. World Health Organization. Traditional medicine growing needs and potential. Geneva: World Health Organization; 2002.No.2.
2
3. Saeidnia S, Yassa N, Rezaeipoor R, Shafiee A, Gohari AR, Kamalinejad M, et al. Immunosuppressive principles from Achillea talagonica, an endemic species of Iran. Daru 2009; 17:37-41.
3
4. Benedek B, Kopp B, Melzig MF. Achillea millefolium L. s.l. is the anti-inflammatory activity mediated by protease inhibition? J Ethnopharmacol 2007; 113:312-317.
4
5. Candan F, Unlu M, Tepe B, Daferera D, Polissiou M, Sokmen A, Akpulat HA. Antioxidant and antimicrobial activity of the essential oil and methanol extracts of Achillea millefolium subsp. millefolium Afan. (Asteraceae). J Ethnopharmacol 2003; 87:215-220.
5
6. Stojanovic G, Radulovic N, Hashimoto T, Palic R. In vitro antimicrobial activity of extracts of four Achillea species: the composition of Achillea clavennae L. (Asteraceae) extract. J Ethnopharmacol 2005; 101:185-190.
6
7. Asgary S, Naderi GH, Sarrafzadegan N, Mohammadifard N, Mostafavi S, Vakili R. Antihypertensive and antihyperlipidemic effects of Achillea wilhelmsii. Drugs Exp Clin Res 2000; 26:89-93.
7
8. Tozyo T, Yoshimura Y, Sakurai K, Uchida N, Takeda Y, Nakai H, et al. Antitumor sesquiterpenoids in Achillea millefolium. Chem Pharm Bull (Tokyo) 1994; 42:1096-100.
8
9. Csupor-Löffler B, Hajdú Z, Zupkó I, Réthy B, Falkay G, Forgo P, et al. Antiproliferative effect of flavonoids and sesquiterpenoids from Achillea millefolium s.l. on cultured human tumour cell lines. Phytother Res 2009; 23:672-676.
9
10. Nemeth E, Bernath J. Biological activities of yarrow species (Achillea spp.). Curr Pharm Des 2008; 14:3151-3167.
10
11. Lemmens-Gruber R, Marchart E, Rawnduzi P, Engel N, Benedek B, Kopp B. Investigation of the spasmolytic activity of the flavonoid fraction of Achillea millefolium s.l. on isolated guinea-pig ilea. Arzneimittelforschung 2006; 56:582-588.
11
12. Yaeesh S, Jamal Q ,Khan AU, Gilani AH. Studies on hepatoprotective, antispasmodic and calcium antagonist activities of the aqueous-methanol extract of Achillea millefolium. Phytother Res 2006; 20:546-551.
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13. Karamenderes C, Apaydin S. Antispasmodic effect of Achillea nobilis L. subsp. sipylea (O. Schwarz) Bässler on the rat isolated duodenum. J Ethnopharmacol 2003; 84:175-179.
13
14. Benedek B, Geisz N, Jager W, Thalhammer T, Kopp B. Choleretic effects of yarrow (Achillea millefolium s.l.) in the isolated perfused rat liver. Phytomedicine 2006; 13:702-706.
14
15. Cavalcanti AM, Baggio CH, Freitas CS, Rieck L, de Sousa RS, Da Silva-Santos JE, et al. Safety and antiulcer efficacy studies of Achillea millefolium L. after chronic treatment in Wistar rats. J Ethnopharmacol 2006; 107:277-2784.
15
16. Mahady GB, Pendland SL, Stoia A, Hamill FA, Fabricant D, Dietz BM, et al. In vitro susceptibility of Helicobacter pylori to botanical extracts used traditionally for the treatment of gastrointestinal disorders. Phytother Res 2005; 19:988-9891.
16
17. Dokhani S, Cottrell T, Khajeddin J, Mazza G. Analysis of aroma and phenolic components of selected Achillea species. Plant Foods Hum Nutr 2005; 60:55-62.
17
18. Afsharypuor S, Asgary S, Lockwood GB. Constituents of the essential oil of Achillea wilhelmsii from Iran. Planta Med 1996; 62:87-78.
18
19. Gherase F, Spac A, Dorneanu V, Stănescu U, Grigorescu E. Pharmacognostic research of some species of Achillea. Note 1. Volatile oils analysis. Rev Med Chir Soc Med Nat Iasi 2003; 107:188-191. (Article in Romanian)
19
20. Javidian K, Miri R, Sadeghpour H. Compsition of the volatile oil of Achillea wilhelmsii C. Koch from Iran. Daru 2004; 12:63-66.
20
21. Nabavizadeh Rafsanjani F, Vahedian J. The effect of insulin-dependent diabetes mellitus on basal and distention-induced gastric acid and pepsin secretion in rat. Diabetes Res Clin Pract 2004; 66:1-6.
21
22. Niazmand S, Hosaini KH, Derakhshan M. The effects of Ziziphora clinopodioides Lam. extract on rat’s gastric motility at basal and vagal stimulated conditions.Pharmacologyonline (newsletter) 2009; 2:734-740
22
23. Rotondo A, Serio R, Mulè F. Gastric relaxation induced by apigenin and quercetin: analysis of the mechanism of action. Life Sci 2009; 85:85-90.
23
24. Wells RW, Lourenssen S, Blennerhassett MG. Impaired acetylcholine-induced smooth muscle contraction in colitis involves altered calcium mobilization and AKT phosphorylation. Pflugers Arch 2008; 456:507-517.
24
25. Bergner A, Sanderson MJ. Acetylcholine-induced calcium signaling and contraction of airway smooth muscle cells in lung slices. J Gen Physiol 2002; 119:187-198.
25
ORIGINAL_ARTICLE
Evaluation of Antioxidants in Bone Mineral Density of Iranian Osteoporotic Women
Objective(s)
Bone is a dynamic tissue that is continuously renewed throughout life by the process of bone remodeling. Antioxidant system might be involved in the pathogenesis of bone loss, so the aim of this study was to evaluate the total antioxidant capacity (TAC), vitamin C and vitamin E levels of plasma besides measuring enzymatic antioxidants, superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) enzymes activity in Iranian osteoporotic women comparing to the control group.
Materials and Methods
Bone mineral density (BMD) of the femoral neck and lumbar spine was measured by dual x-ray absorptiometry. The participants were divided into groups: a) total participants (-3.9 ≤ T–score ≤ 3.6) including 192 women, b) the control group (T-score ≥ -1) including 76 women, c) the total patients (T-score < -1) including 76 women. Then, plasma TAC, vitamin C levels, SOD and GR activities, erythrocyte CAT were measured using spectrophotometrical methods separately, and for vitamin E by HPLC analysis.
Results
Comparing the control group and osteoporotic women showed that: a) plasma levels for vitamin C and erythrocyte CAT were markedly lower in the patients than in the controls, but plasma activity of TAC, SOD and GR were significantly higher, respectively. b) the differences were higher between control and patients with severe disease (T-score <-1.7) comparing to patients in the group with milder disease (-1.7 ≤ T-score <-1). c) Femoral neck BMD adjusted with age and BMI showed a positive and significant correlation with plasma levels of vitamin C in all subjects, but this relation was reverse or negative for TAC, SOD and GR.
Conclusion
It seems that a physiologic increase in the amount of some antioxidants occurs in osteoporosis; even though this amount may not be sufficient for the human body requirements.
https://ijbms.mums.ac.ir/article_4982_b94641d69e10f63c7ba040cd762a3ad9.pdf
2011-03-01
158
166
10.22038/ijbms.2011.4982
Antioxidants
Blood
Bone Density
Osteoporosis
Women
Mohammad Reza
Oveisi
1
Department of Drug and Food Control, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Naficeh
Sadeghi
nsadeghi@sina.tums.ac.ir
2
Department of Drug and Food Control, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Behrooz
Jannat
janatbhr@sina.tums.ac.ir
3
Food and Drug Laboratory Research Center, Ministry of Health and Medical Education, Tehran, Iran
LEAD_AUTHOR
Mannan
Hajimahmoodi
4
Department of Drug and Food Control, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Molouk
Hadjibabaie
5
Pharmacotherapy Department, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran
AUTHOR
Abdolazim
Behfar
aa_behfar@yahoo.com
6
Drug and Food Control Department, Faculty of Pharmacy, Jondishapoor University of Medical Sciences, Ahvaz, Iran
AUTHOR
1. Thomas E, Andreoli Charles CJ, Carpenter RC, Griggs Jl. Cecil essentials of medicine. Philadelphia: W.B.Saunders Company; 2004.
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2. Mundy GR. Bone Remodeling. In: MJ F.editor. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. New York: Lippincott, Williams & Wilkins;1999.p.30-38.
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3. Chan GK, Duque G. Age-related bone loss: old bone, new facts. Gerontology 2002; 48:62-71.
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4. The abstract book of the first international seminar on prevention, diagnosis and treatment of osteoporosis. Endocrinol Metab Res Center 2004; 23-24
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5. Bartl R, Frisch B. Recognizing Risk Factors Osteoporosis: Diagnosis, prevention, therapy. New York: Springer- Verlag; 2004.
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6. Rao LG. Will Tomatoes Prevent Osteoporosis? Endocrinology Rounds 2005; 5: 2.
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7. Sahnoun Z, Jamoussi K, Zeghal KM. Free radicals and antioxidants:human physiology, pathology and therapeutic aspects. Therapie 1997; 52:251-270.
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8. Knight JA.The biochemistry of aging .Adv Clin Chem 2000; 35:1-62.
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9. McCormick RK.Osteoporosis: integrating biomarkers and other diagnostic correlates into the management of bone fragility.. Alternative Medicine Review 2007; 12: 113-145.
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10. Melhus H, Michaelsson K, Holmberg L, Wolk A, Ljunghall S. Smoking, antioxidant vitamins, and the risk of hip fracture. J Bone Miner Res 1999; 14:129-135.
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11. Morton DJ, Barrett-Connor EL, Schneider DL.Vitamin C supplement and bone mineral density in postmenopausal women. J Bone Miner Res 2001; 16:135-140.
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12. Ozgocmen S, Kaya H, Fadillioglu E, Aydogan R, Yilmaz Z. Role of antioxidant systems, lipid peroxidation, and nitric oxide in postmenopausal osteoporosis. Mol Cell Biochem 2007; 295:45-52.
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13. Fatokum AA, Stone TW, Smith RA . Response of different MC3T3-E1 osteoblast – like cells to reactive oxygen species. Eur J Pharm 2008; 587:35-41.
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14. Benzie IFF, Strain JJ. The ferric reducing ability of plasma as a power: The FRAP assay. Anal Bio Chem 1999; 239:70-76.
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15. Hajimahmoodi M, Mojtahedzadeh M, GhaffarNatanzi N, Sadrai S, Sadeghi N, Nadjafi A, et al. Effects of vitamin E administration on APACHE II Score in ARDS patients. Daru 2009; 17:24-28.
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16. Chung WY, Chung JKO, Szeto YT, Tomlinson B, Benzie IFF.Plasma ascorbic acid: measurement, stability and clinical utility revisited. Clin Biochem 2001; 34: 623-627.
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17. Aebi HE. Catalase:hydrogen-peroxide oxidoreductase. In:Bergmeyer HU, Bergmeryer J, Greassl M, editors. Methods of enzymatic analysis. Weinhemi: Verlag Chemie 1983.p. 273-285.
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18. Elstner EF, Youngamn RJ, Osswld W. Superoxide dismutase. In: Bergmeyer HU, Bergmeryer J, Greassl M, ed. Methods of enzymatic analysis. Weinhemi: Verlag Chemie 1983.p.293-302.
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19. Goldberg DM, Spooner RJ. Oxidoreductases acting on groups other than CHOH. Glutathione reductase.In: Bergmeyer HU, Bergmeyer J, Grassl M,editors.In Methods of Enzymatic Analysis.Verlag Chemie, Weinheim 1983.p.258-265.
19
20. Basu S, Michaelsson K, Olofsson H, Johansson S, Melhus H. Association between oxidative stress and bone mineral density. Biochem Biophys Res Commun 2001; 288:275-279.
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21. Sontakke AN, Tare RS. A duality in the roles of reactive oxygen species with respect to bone metabolism. Clin Chim Acta 2002; 318:145-148.
21
22. Sadeghi N, Oveisi MR, Jannat B, Hajimahmoodi M, Jamshidi AR, Sajadian Z. Determination of plasma gluthatione reductase enzyme activity in osteoporotic women. Daru 2008; 19:51-54.
22
23. Behfar AA, Sadeghi N, Oveisi MR, Jannat B, Hajimahmoodi M, Jamshidi AR, et al. The plasma antioxidant activity of superoxide dismutase enzyme in osteoporosis. Acta Med Iran 2008; 46:441-446.
23
24. Maggio D, Barabani M, Pierandrei M, Polidori MC, Catani M, Mecocci P, et al. Marked decrease in plasma antioxidants in aged osteoporotic women: results of a cross-sectional study. J Clin Endocrinol Metab 2003; 88:1523-1527.
24
25. Bax BE, Alam AS, Banerji B.Stimulation of osteoclastic bone resorption by hydrogen peroxide. Biochem Biophys Res Commun 19992; 183:1153-1158.
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26. Suda N, Morita I, Kuroda T, Murota S.Participation of oxidative stress in the process of osteoclast differentiation. Biochim Biophys Acta 1993; 1157:318-323.
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27. Steinbeck MJ, Kim JK, Trudeau MJ, Hauschka PV, Karnovsky MJ. Involvement of hydrogen peroxide in the differentiation of clonal HD-11EM cells into osteoclast-like cells. J Cell Physiol 1998; 176:574-587.
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28. Nam SH, Jung SY, Yoo CM, Ahn EH, Suh CK. H2O2 enhances Ca2+ release from osteoblast internal stores. Yonsei Med J 2002; 43:229-235.
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29. Darden AG, Ries WL, Wolf WC, Rodriguiz RM, Key LL. Osteoclastic superoxide production and bone resorption:stimulation and inhibition by modulators of NADPH oxidase. J Bone Miner Res 1996; 11:671-675.
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30. Soo SJ, Lee KW, Rhee JS, Hwang DS, Lee YM, Park HG, et al. Environmental stressors (salinity, heavy metals and H2O2) modulate expression of glutathione reductase (G R) gene from theintertidal copepod tigriopus japonicus. Aquat Toxicol 2006; 80:281-289.
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31. Diplock AT. Antioxidant nutrients and disease prevention: an overview. Am J Clin Nutr 1999; 53:189-193.
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32. Buttner GR, Jurkiewicz BA.Catalytic metals, Ascorbate and free radicals: Combinations to avoid. Radiat Res 1996; 145:532-541.
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33. Roughead ZK, Kunkel ME. Effect of diet on bone matrix constituents. J Am Coll Nutr 1991; 10:242-246.
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34. Franceschi RT. The role of ascorbic acid in mesenchymal differentaion. Nutr Rev 1992; 50:65-70.
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35. Francesschi R, Iyer B. Relationship between collgen synthesis and expression of the ostesblast phenotype in Mc3T3-E1 cells. J Bone Miner Res 1992; 7:235-246.
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36. Ostalowska A, Birkner E, Wiecha M, Kasperczyk S, Kasperczyk A, Kapolka D, et al. Lipid peroxidation and antioxidant enzymes in synovial fluid of patients with primary and secondary osteoarthritis of the knee joint. Osteoarthritis Cartilage 2006; 14:139-145.
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37. Sacheck JM, Blumberg JB. Role of vitamin E and oxidative stress in exercise. Nutrition 2001; 17:809-814.
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38. Wolf RL, Cauley JA, Pettinger M, Jackson R, Lacroix A, Leboff MS, et al. Lack of a relation between vitamin and mineral antioxidants and bone mineral density: results from the Women's Health Initiative.Am J Clin Nutr 2005; 82:581-588.
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39. Cherubini A, Polidori MC, Bregnocchi M, Pezzuto S, Cecchetti R, Ingegni T, et al. Antioxidant profile and early outcome in stroke patients. Stroke 2000; 31:2295-2300.
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40. Polidori MC, Stahl W, Eichler O, Niestroj I, Sies H. Profiles of antioxidants in human plasma. Free Radic Biol Med 2001; 30:456-462.
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41. Kimura F, Hasegawa G, Obayashi H, Adachi T, Hara H, Ohta M, et al. Serum extracellular superoxide dismutase in patients with type 2 diabetes: relationship to the development of micro- and macro vascular complications. Diabetes Care 2003; 26:1246-1250.
41
ORIGINAL_ARTICLE
Blockade of the Naloxone-induced Aversion in Morphine-conditioned Wistar Rats by L-Arginine Intra-central Amygdala
Objective(s)
Single injection of naloxone, a selective antagonist of morphine, prior to the drug conditioning testing was used to investigate on morphine dependence.
Materials and Methods
Conditioning to morphine (2.5-10 mg/kg, s.c.) was established in adult male Wistar rats (weighing 200-250 g) using an unbiased procedure. Nitric oxide agents were microinjected into the central amygdala prior to naloxone-paired place conditioning testing.
Results
The results showed that morphine produced a significant dose-dependent place preference in animals. Naloxone (0.1-0.4 mg/kg, i.p.) injections pre-testing of the response to morphine (7.5 mg/kg, s.c.) caused a significant aversion at the higher doses (0.4 mg/kg, i.p.). This response was reversed by microinjection of L-arginine (0.3-3 μg/rat, intra-central amygdala) prior to naloxone on the day of the testing. The response to L-arginine was blocked by pre-injection of NG-nitro-L-arginine methyl ester (L-NAME) (intra-central amygdala).
Conclusion
A single injection of naloxone on the test day of morphine place conditioning may simply reveal the occurrence of morphine dependence in rats, and that the nitric oxide in the central amygdala most likely plays a key role in this phenomenon.
https://ijbms.mums.ac.ir/article_4983_654328bfa15d999734fb69d7c9578cf5.pdf
2011-03-01
167
176
10.22038/ijbms.2011.4983
Amygdala
Morphine dependence
Naloxone
Nitric oxide
Mahnaz
Rahimpour
1
MS student, Department of Biology, Faculty of Basic Sciences, Shahed University, Tehran, Iran
AUTHOR
Manizheh
Karami
karami@shahed.ac.ir
2
Department of Biology, Faculty of Basic Sciences, Shahed University, Tehran, Iran
LEAD_AUTHOR
Sara
Karimi
3
MS student, Department of Biology, Faculty of Basic Sciences, Shahed University, Tehran, Iran
AUTHOR
Abbas
Haghparast
haghparast@yahoo.com
4
Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
AUTHOR
Mohammad Reza
Jalali
5
Department of Pathology, School of Medicine, Shahed University, Tehran, Iran
AUTHOR
Farzaneh
Sabouni
saboni@nigeb.ac.ir
6
National Institute of Genetic Engineering and Biotechnology, Tehran, Iran
AUTHOR
1. Gutstein HB, Akil H. Opioid analgesics. In: Hardman JG, Limbird LE, Goodman Gilman A, editors. Goodman and Gilman’s the Pharmacological Basis of Therapeutics.10th ed. New York: McGraw-Hill; 2001.p.569-619.
1
2. Karami M, Zarrindast MR. Morphine sex-dependently induced place conditioning in adult Wistar rats. Eur J Pharmacol 2008; 582:78-87.
2
3. McClung CA. The molecular mechanisms of morphine addiction. Rev Neurosci 2006; 17: 393-402.
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4. Watanabe T, Nakagawa T, Yamamoto R, Maeda A, Minami M, Satoh M. Involvement of glutamate receptors within the central nucleus of the amygdala in naloxone-precipitated morphine withdrawal-induced conditioned place aversion in rats. Jpn J Pharmacol 2002; 88: 399-406.
4
5. Watanabe T, Nakagawa T, Yamamoto R, Maeda A, Minami M, Satoh M. Involvement of noradrenergic system within the central nucleus of the amygdala in naloxone-precipitated morphine withdrawal-induced conditioned place aversion in rats. Sychopharmacol (Berl) 2003; 170: 80-88.
5
6. Ikemoto S. Dopamine reward circuitry: two projection systems from the ventral midbrain to the nucleus accumbens-olfactory tubercle complex. Brain Res Rev 2007; 56:27-78.
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7. Spanagel R, Weiss F. The dopamine hypothesis of reward: past and current status. Trends Neurosci 1999; 22:521-527.
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8. Wise RA. Drug-activation of brain reward pathways. Drug Alcohol Depend 1998; 51:13-22.
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9 Di Chiara G, North RA. Neurobiology of opiate abuse. Trends Pharmacol Sci 1992; 13:185-193.
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10. Bardo MT, Bevins RA. Conditioned place preference: what does it add to our preclinical understanding of drug reward? Psychopharmacology (Berl) 2000; 153:31-43.
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13. Tzschentke TM. Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade. Addict Biol 2007; 12:227-462.
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15. Vargas-Perez H, Ting-A-Kee R, van der Kooy D. Different neural systems mediate morphine reward and its spontaneous withdrawal aversion. Eur J Neurosci 2009; 29:2029-2034.
13
16. Wise RA. The role of reward pathways in the development of drug dependence. Pharmacol Ther 1987: 35:227- 263.
14
17. Zarrindast MR, Karami M, Sepehri H, Sahraei H. Influence of nitric oxide on morphine-induced conditioned place preference in the rat central amygdala. Eur J Pharmacol 2002; 453: 81-89.
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18. Crain SM, Shen KF. Ultra-low concentrations of naloxone selectively antagonize excitatory effects of morphine on sensory neurons, thereby increasing its anti-nociceptive potency and attenuating tolerance/dependence during chronic co-treatment. Proc Natl Acad Sci USA 1995; 92:10540-10544.
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19. Wang H-Y, Friedman E, Olmstead MC, Burns LH. Ultra-low-dose naloxone suppresses opioid tolerance, dependence and associated changes in mu-opioid receptor-G protein coupling and Gbetagamma signaling. Neuroscience 2005; 135:247-261.
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20. Zheng-xiong XI, Stein EA. Gabaergic mechanisms of opiate reinforcement. Alcohol 2002; 37:485-494.
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21. Di Chiara G, Imperato A. Drugs abused by humans preferentially increase synaptic dopamine concentrations in the mesolimbic system of freely moving rats. Proc Natl Acad Sci USA 1988; 85:5274-5278.
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22. Olmstead MC, Franklin KB. Development of a conditioned place preference: effects of lesions of various CNS sites. Behav Neurosci 1997; 111:1313-23.
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24. Diaz SL, Barros VG, Antonelli MC, Rubio MC, Balerio GN. Morphine withdrawal syndrome and its prevention with baclofen: Autoradiographic study of mu-opioid receptors in prepubertal male and female mice. Synapse 2006; 60:132-140.
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26. Fukuto JM, Mayer B. The enzymology of nitric oxide synthase. In: Feelisch M, Stamler JS, editors. Methods in nitric oxide research. New York: John Wiley & Sons Ltd; 1996. p. 147-157.
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31. Haghparast A, Azizi P, Hassanpour-Ezatti M, Khorrami H, Naderi N. Sub-chronic administration of AM251, CB1 receptor antagonist, within the nucleus accumbens induced sensitization to morphine in the rat. Neurosci Lett 2009; 467:43-47.
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33. Moaddab M, Haghparast A, Hassanpour-Ezatti M. Effects of reversible inactivation of the ventral tegmental area on the acquisition and expression of morphine-induced conditioned place preference in the rat. Behav Brain Res 2009; 198:466-471.
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36. Heinmiller A, Ting-A-Kee R, Vargas-Perez H, Yeh A, van der Kooy D. Tegmental pedunculopontine glutamate and GABA-B synapses mediate morphine reward. Behav Neurosci 2009; 123:145-155.
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37. Skoubis PD, Matthes HW, Walwyn WM, Kieffer BL, Maidment NT. Naloxone fails to produce conditioned place aversion in mu-opioid receptor knock-out mice. Neuroscience 2001; 106:757-763.
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39. Bozarth MA. Conditioned place preference. A parametric analysis using systemic heroin injections. In: Bozarth MA, editor. Methods of assessing the reinforcing properties of abused drugs. New York: Springer- Verlag;1987.p.241-273.
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48
ORIGINAL_ARTICLE
Evaluation of Origanum Vulgare L. ssp. Viridis Leaves Extract Effect on Discrimination Learning and LTP Induction in the CA1 Region of the Rat Hippocampus
Objective(s) The objective of this study was to determine the effect of aqueous extract of Origanum vulgare L. ssp. Viridis (ORG) on discrimination learning and long term potentiation (LTP) in CA1 region of the rat hippocampus. Materials and Methods A group of adult male Wistar rats weighing 275±25 g received aqueous extract of ORG (150, 300, 450 mg/kg/day) by intraperitoneal injection for one week, and the other group received saline (n= 6). A wooden T-maze was used to evaluate the discrimination learning. In electrophysiological experiments, the effect of ORG leaves extract on induction and maintenance of long term potentiation (LTP) in CA1 hippocampus area was determined. LTP was evaluated in CA1 region after high-frequency stimulation (200 Hz) of the Schaffer collaterals. Also, serum antioxidant levels were analyzed in the two groups (n= 4). Results Statistical analysis showed significant decreases in the number of total (significantly at the dose of 300 and 450 mg/kg) and wrong (significantly at the dose of 300 mg/kg) entrance into opposite box of T-maze procedure in ORG-treated animals (P< 0.05). In electrophysiological study, the rats which had received ORG (150, 300, and 450 mg/kg) showed an increase in both population spike amplitude (59.7±14.1%, 85±14.7% and 49.3±8.7% respectively, compared to 39±9.2% increase in saline group) and maintenance of LTP in hippocampus CA1 after high frequency stimulation in Schaffer collateral pathway. In serum antioxidant assay, level of antioxidants in ORG groups (300 and 450 mg/kg) remarkably increased in comparison to saline group (P< 0.05 and P< 0.001, in turn). Conclusion Our results suggest that Origanum aqueous extract can improve the learning criteria in rats.
https://ijbms.mums.ac.ir/article_4984_0d34343e895bdc9d97b9ddf49dcbc7ae.pdf
2011-03-01
177
184
10.22038/ijbms.2011.4984
Antioxidant assay
Long term potentiation
Medicinal plant
Origanum vulgare
Spatial learning
T-maze
Vahid
Sheibani
vsheibani2@yahoo.com
1
Kerman Neuroscience Research Center, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Mohammadreza
Afarinesh
reza.afarinesh@gmail.com
2
Kerman Neuroscience Research Center, Kerman University of Medical Sciences, Kerman, Iran
LEAD_AUTHOR
Zahra
Hajializadeh
hajializadeh.z@yahoo.com
3
Kerman Neuroscience Research Center, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Mehdi
Abbasnejad
mabbas@uk.ac.ir
4
Biology Department of Shahid Bahonar University of Kerman, Kerman, Iran
AUTHOR
Tahereh
Haghpanah
tara_hagh2000@yahoo.com
5
Kerman Neuroscience Research Center, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Razieh
Arabnezhad
6
Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
Gholamreza
Sepehri
7
Kerman Neuroscience Research Center, Kerman University of Medical Sciences, Kerman, Iran
AUTHOR
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45
ORIGINAL_ARTICLE
Assessment of VEGF, CD-31 and Ki-67 Immunohistochemical Markers in Oral Pyogenic Granuloma: A Comparison with Hemangioma and Inflammatory Gingivitis
Objective(s)
The aim of this study was to evaluate the expressions of two angiogenic immune-markers (CD-31 and VEGF), and one proliferative immune-marker (Ki-67) in oral pyogenic granulomas (PG), hemangiomas (Hem) and inflammatory gingivitis (IG).
Materials and Methods
Sixty cases of PG, Hem and IG (twenty cases each) were examined. Immunohistochemical (IHC) staining was performed based on routine techniques. The microvessel density (MVD) index was also evaluated.
Results
The male to female ratio was 1:2. The mean age was 33.3 years old (±20.52). The reactivity percentages for all three markers (CD-31, VEGF and Ki-67) were significantly higher in PG compared to Hem (56.8%, 13.8% and 23.0% vs. 28.3%, 7.0% and 5.4%, respectively). The mean MVD in PG was also significantly higher than in Hem (26.1±0.11 vs. 13.6±0.08). There was no statistically significant difference between PG and IG.
Conclusion
The current study supports the common nature of pyogenic granulomas and inflammatory gingivitis.
https://ijbms.mums.ac.ir/article_4985_e83d4ff38119d9147f96645a331e99a7.pdf
2011-03-01
185
189
10.22038/ijbms.2011.4985
CD31
Gingivitis
Hemangioma
Ki-67 Antigen
Pyogenic Granuloma
VEGF
Shadi
Saghafi
saghafis@mums.ac.ir
1
Department of Oral Pathology, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Sakineh
Amoueian
amouians@mums.ac.ir
2
Imam-Reza Hospital, Mashhad University of Medical Sciences, Mashhad, Iran
LEAD_AUTHOR
Mehdi
Montazer
3
Department of Pathology, Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
Roshanak
Bostan
4
Mashhad University of Medical Sciences, Mashhad, Iran
AUTHOR
1.Cohen M, Michel Jr. Vasculogenesis angiogenesis, hemangiomas, and vascular malformations. Am J Med Genet 2002; 108:265- 274.
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2. Jafarzaddeh H, Sanatkhani M, Mohtasham N. Oral pyogenic granuloma: a review. J Oral Sci 2006; 48:167-175.
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3.Dyduch G, Okoń K, Mierzyński W. Benign vascular proliferations--an immunohistochemical and comparative study. Pol J Pathol 2004; 55:59-64.
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4.Dyduch G, Okoń K. Proliferation and apoptosis within the oral mucosa "hemangiomas". Pol J Pathol 2000; 5193-96.
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5. Nakamura T. Apoptosis and expression of Bax/Bcl-2 proteins in pyogenic granuloma: a comparative study with granulation tissue and capillary hemangioma. J Cutan Pathol 2000; 27:400–405.
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6. Freitas TM, Miguel MC, Silveira EJ, Freitas RA, Galvão HC. Assessment of angiogenic markers in oral hemangiomas and pyogenic granulomas. Exp Mol Pathol 2005; 79:79-85.
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10. Toida M, Hasegawa T, Watanabe F, Kato K, Makita H, Fujitsuka H, et al. Lobular capillary hemangioma of the oral mucosa: clinicopathological study of 43 cases with a special reference to immunohistochemical characterization of the vascular elements. Pathol Int 2003; 53:1-7.
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15