@article { author = {Malaekeh-Nikouei, Bizhan and Arabi, Leila and Roohbakhsh, Ali and Fazly Bazzaz, BiBi Sedigheh}, title = {Iranian Journal of Basic Medical Sciences, comparison of the three recent years}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {1-2}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.19401}, abstract = {}, keywords = {}, url = {https://ijbms.mums.ac.ir/article_19401.html}, eprint = {https://ijbms.mums.ac.ir/article_19401_af2f61033cedbe0f5da9835295196bb5.pdf} } @article { author = {Rahimi, Hamid Reza and Mojarad, Majid and Moghbeli, Meysam}, title = {MicroRNA-96: A therapeutic and diagnostic tumor marker}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {3-13}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.59604.13226}, abstract = {Cancer has been always considered as one of the main human health challenges worldwide. One of the main causes of cancer-related mortality is late diagnosis in the advanced stages of the disease, which reduces the therapeutic efficiency. Therefore, novel non-invasive diagnostic methods are required for the early detection of tumors and improving the quality of life and survival in cancer patients. MicroRNAs (miRNAs) have pivotal roles in various cellular processes such as cell proliferation, motility, and neoplastic transformation. Since circulating miRNAs have high stability in body fluids, they can be suggested as efficient noninvasive tumor markers. MiR-96 belongs to the miR-183-96-182 cluster that regulates cell migration and tumor progression as an oncogene or tumor suppressor by targeting various genes in solid tumors. In the present review, we have summarized all of the studies that assessed the role of miR-96 during tumor progression. This review clarifies the molecular mechanisms and target genes recruited by miR-96 to regulate tumor progression and metastasis. It was observed that miR-96 mainly affects tumorigenesis by targeting the structural proteins and FOXO transcription factors.}, keywords = {Cancer,Diagnosis,MicroRNA,miR-96,Prognosis}, url = {https://ijbms.mums.ac.ir/article_19434.html}, eprint = {https://ijbms.mums.ac.ir/article_19434_ff7fa24f14ea56f74a3406f162818d35.pdf} } @article { author = {Hu, Zhihua and Guan, Yurong and Hu, Wanying and Xu, Zhiyong and Ishfaq, Muhammad}, title = {An overview of pharmacological activities of baicalin and its aglycone baicalein: New insights into molecular mechanisms and signaling pathways}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {14-26}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2022.60380.13381}, abstract = {The flavonoids, baicalin, and its aglycone baicalein possess multi-fold therapeutic properties and are mainly found in the roots of Oroxylum indicum (L.) Kurz and Scutellaria baicalensis Georgi. These flavonoids have been reported to possess various pharmacological properties, including antibacterial, antiviral, anticancer, anticonvulsant, anti-oxidant, hepatoprotective, and neuroprotective effects. The pharmacological properties of baicalin and baicalein are due to their abilities to scavenge reactive oxygen species (ROS) and interaction with various signaling molecules associated with apoptosis, inflammation, autophagy, cell cycle, mitochondrial dynamics, and cytoprotection. In this review, we summarized the molecular mechanisms underlying the chemopreventive and chemotherapeutic applications of baicalin and baicalein in the treatment of cancer and inflammatory diseases. In addition, the preventive effects of baicalin and baicalein on mitochondrial dynamics and functions were highlighted with a particular emphasis on their anti-oxidative and cytoprotective properties. The current review highlights could be useful for future prospective studies to further improve the pharmacological applications of baicalein and baicalin. These studies should define the threshold for optimal drug exposure, dose optimization and focus on therapeutic drug monitoring, objective disease markers, and baicalin/baicalein drug levels. }, keywords = {Baicalein,Baicalin,Cancer,Inflammatory diseases,Mitochondrial functions}, url = {https://ijbms.mums.ac.ir/article_19489.html}, eprint = {https://ijbms.mums.ac.ir/article_19489_2ad0459f107121aff4b93a0478ef9dd6.pdf} } @article { author = {Hosseininejad-Chafi, Mohammad and Alirahimi, Ehsan and Ramezani, Behzad and Oghalaei, Akbar and Sotoudeh, Nazli and Ghaderi, Hajarsadat and Kazemi-Lomedasht, Fatemeh and Habibi-Anbouhi, Mahdi and Moazzami, Reza and Behdani, Mahdi}, title = {In vivo solid tumor targeting with recombinant VEGF-diphtheria immunotoxin}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {27-31}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.54293.12195}, abstract = {Objective(s): A variety of signaling molecules have been identified that play a role in angiogenesis, of prime importance, vascular endothelial growth factor (VEGF) and its resceptor (VEGFR), which is highly expressed in most human solid tumors. Targeting VEGF or/and VEGFR with immunotoxin may be a promising approach to directly affect cancer cells. Immunotoxins are for targeted treatment comprising two functional moieties, an antibody that binds to target cells along with toxin that kills molecules.  Materials and Methods: In this study, an immunotoxin comprising domain of diphtheria toxin subunit A (DT386) genetically fused to mouse VEGF (mVEGF-DT) was developed. The second construct, which contains the DT386 domain, was made to investigate the action of the DT386 domain on tumor cells. Both gene constructs were cloned, expressed, and were further purified. The biological activity of mVEGF-DT and DT386 proteins was assessed on the TC1 cell line bearing mouse model. Proteins were injected intra-tumoral in mice, in separate groups. Results: Tumors in the mVEGF-DT group started to dwindle after six injections, but tumor size in both control groups (DT386 and PBS), continued to grow. Conclusion: Successful targeting of solid tumor cells by mVEGF-DT immunotoxin demonstrates the therapeutic potential utility of these conjugates for tumor targeting.}, keywords = {Angiogenesis,Immunotherapy,Immunotoxin,Tumor,Vascular endothelial growth - factor (VEGF)}, url = {https://ijbms.mums.ac.ir/article_19108.html}, eprint = {https://ijbms.mums.ac.ir/article_19108_6007af86ddcf194520f441d519302e32.pdf} } @article { author = {Zonnar, Saghar and Saeedy, Said Abdul Ghafour and Nemati, Fahimeh and Motamedi, Mohammad Javad and Raeespour, Hamidreza and Amani, Jafar}, title = {Decrescent role of recombinant HSP60 antibody against atherosclerosis in high-cholesterol diet immunized rabbits}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {32-38}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.56382.12580}, abstract = {Objective(s): Atherosclerosis is the main cause of cardiovascular disease (CVD) which has a key role in the development of coronary artery disease (CAD). Based on clinical studies, HSP60 is the only HSP that can cause atherosclerosis. In this paper, the expression level of HSP60 and the pathogenic degree of its cloned part was investigated in atherosclerosis condition.Materials and Methods:  After the designation of the specific primers for HSP60, PCR was done by the Pfu enzyme. Subsequently, the PCR products were cloned into a prokaryotic expression vector pET-28a. The resultant recombinant vector was transferred in BL21 and purified. Purification of protein was done by the Nickel affinity column. After confirmation of Western blotting and HSP60 protein purification, purified protein concentration was measured by the Bradford method, and purity was analyzed by SDS PAGE 12%. New Zealand rabbits were tested as an animal model. At the next step, the recombinant protein was injected into the animal model that was on a fatty diet.Results: The prokaryotic expression plasmid pET28a-hps60 was successfully constructed, the HSP60 protein was expressed and purified in Escherichia coli BL21 (DE3). We found that the rabbit that was receiving the recombinant vaccine with the fatty diet showed a lower amount of fat deposition at the media endothelial level than the rabbit which received only the fatty diet. Conclusion: Taking recombinant protein concomitant with a fatty diet, causes betterment of atherosclerosis via decreasing aggregation of cholesterol and thickness of the endothelial media.}, keywords = {Atherosclerosis,Coronary Artery Disease,Heat- shock proteins,Plasmids,Recombinant protein}, url = {https://ijbms.mums.ac.ir/article_19302.html}, eprint = {https://ijbms.mums.ac.ir/article_19302_fb8baf1f7f078a55a7f44b79af5081cc.pdf} } @article { author = {Fatemi, Iman and Saeed Askari, Pooya and Hakimizadeh, Elham and Kaeidi, Ayat and Esmaeil-Moghaddam, Sogand and Pak-Hashemi, Mohammad and Allahtavakoli, Mohammad}, title = {Chronic treatment with coenzyme Q10 mitigates the behavioral dysfunction of global cerebral ischemia/reperfusion injury in rats}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {39-45}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2022.57630.12865}, abstract = {Objective(s): The Ischemia/reperfusion (I/R) phenomenon has a critical role in brain injuries induced by some kinds of stroke. The current study investigates the effects of Coenzyme Q10 (Q10) on global cerebral I/R in rats. Materials and Methods: Fifty male Wistar rats were used in this study. The global cerebral I/R was induced by obstructing both common carotid arteries for 20 min and the animals were treated with Q10 (200 mg/kg; PO.) for 6 weeks. Depressive and anxiety-like behaviors were assessed using the elevated plus-maze and forced swimming test, respectively. Working and spatial learning and memory were assessed by the Y-maze continuous alternation task and Morris water maze. The brain tissues were evaluated for brain edema, brain-derived neurotrophic factor (BDNF) levels, and superoxide dismutase (SOD) activities. Results: Our results indicated that global cerebral I/R increased anxiety and depression-like behavior as well as reduced cognitive performance. Moreover, the levels of BDNF and activities of SOD are reduced in stroke animals. Chronic post-stroke treatment with Q10 decreased brain edema. Furthermore, Q10 administration reduced anxiety and depressive-like behavior as well as cognitive impairments in stroke animals. Q10 also increased the SOD activities and BDNF levels in the brain tissues of stroke animals. Conclusion: Finally, we can conclude that using Q10 supplementation may be beneficial against the global cerebral I/R complications.}, keywords = {Brain Injuries,Free radicals,Ischemia/Reperfusion,Q10,Rat}, url = {https://ijbms.mums.ac.ir/article_19479.html}, eprint = {https://ijbms.mums.ac.ir/article_19479_633a23e10bdc1197b280a50703e94750.pdf} } @article { author = {Chen, Xiao-Guang and Dou, Bing-Hua and An, Jin-Dou and Feng, Song and Liu, Na and Sheng, Guang-Yao}, title = {MAGI2-AS3 restrains proliferation, glycolysis, and triggers apoptosis in acute lymphoblastic leukemia via regulating miR-452-5p/FOXN3 pathway}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {46-52}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.58963.13095}, abstract = {Objective(s): MAGI2-AS3 is a cancer suppressor gene of multiple malignancies. Acute lymphoblastic leukemia (ALL) is an important type of leukemia that especially occurs in children. Our work evaluated the modulation of MAGI2-AS3 in ALL.Materials and Methods: qPCR and Western blotting were adopted for detection of target molecular expression. Growth and apoptosis were determined by CCK8 assay and Annexin V/PI staining. Glycolysis was detected by commercial kits. The direct binding between miR-452-5p and MAGI2-AS3 or FOXN3 was assessed by luciferase reporter assay. Tumor growth was measured in nude mice in vivo.Results: MAGI2-AS3 was down-regulated in ALL. Enforced expression of MAGI2-AS3 inhibited growth and glycolysis while promoting apoptosis of ALL cells. Moreover, MAGI2-AS3 up-regulated FOXN3 via sponging miR-452-5p. FOXN3 depletion abrogated MAGI2-AS3-mediated anti-cancer action. More importantly, MAGI2-AS3 repressed ALL cell growth in nude mice through regulation of miR-452-5p/FOXN3. Conclusion: MAGI2-AS3 inhibits ALL development via modulating miR-452-5p/FOXN3.}, keywords = {ALL,Apoptosis,FOXN3,Glycolysis,Growth,MAGI2-AS3,miR-452-5p}, url = {https://ijbms.mums.ac.ir/article_19301.html}, eprint = {https://ijbms.mums.ac.ir/article_19301_2880897d75bd5e6d764067c82942d63b.pdf} } @article { author = {Abdanipour, Alireza and Nikfar, Ali and Nikbakht Rad, Mahsa and Jafari Anarkooli, Iraj and Mansouri, Mojdeh}, title = {Neuroprotective effect of L-deprenyl on the expression level of the Mst1 gene and inhibition of apoptosis in rat-model spinal cord injury}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {53-59}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2022.58031.12894}, abstract = {Objective(s): After primary tissue damage as a result of spinal cord injury (SCI), there is a period of secondary damage, which includes several cellular and inflammatory biochemical cascades. As a novel pro-apoptotic kinase, Mst1 (serine/threonine kinase 4) promotes programmed cell death in an inflammatory disease model. This study aimed to evaluate Mst1 gene expression levels in rats with spinal cord injury treated with L- deprenyl. Materials and Methods: The rats were divided into control (contusion), laminectomy, sham-operated (contused rats received 1 ml normal saline intraperitoneal), and treatment (contused rats received 5 mg/kg of L-deprenyl intraperitoneal; once a day for 7 days). The BBB (Basso, Beattie, and Bresnahan) scales were performed to assess motor function following SCI. Rats were sacrificed 28 days after SCI and the spinal cord lesion area was removed. Apoptosis and cavity formation in the spinal cord were determined by H&E staining and TUNEL assay, respectively. The mRNA levels of the Mst1, Nrf2, Bcl-2, and PGC1α genes were analyzed using real-time quantitative PCR.Results: The results showed significant improvement in motor function in the L- deprenyl group compared with the untreated group. Histological analysis showed a significant reduction in the number of tunnel-positive cells after injection of L-deprenyl, as well as a decrease in the volume of the cavity. In addition, L-deprenyl treatment increased the expression of the Nrf2, Bcl-2, and PGC1α genes, while reducing the expression of the Mst1 gene in the spinal nerves. Conclusion: These results suggest that L-deprenyl is a promising treatment for spinal cord injury.}, keywords = {Apoptosis,Bcl-2,Contusion,L-deprenyl,Mst1,Nrf2,Selegiline}, url = {https://ijbms.mums.ac.ir/article_19480.html}, eprint = {https://ijbms.mums.ac.ir/article_19480_9a5658d8ae6cc7da8904e7b6e8653419.pdf} } @article { author = {Amirshahrokhi, Keyvan and Abzirakan, Arezoo}, title = {Carvedilol attenuates acrylamide-induced brain damage through inhibition of oxidative, inflammatory, and apoptotic mediators}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {60-67}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.58808.13063}, abstract = {Objective(s): Acrylamide is a potent neurotoxic compound and has harmful effects on brain cells. Acrylamide promotes oxidative, inflammatory, and apoptotic mediators in the CNS leading to neurological disorders. The goal of the current study was to examine the potential protective effect of carvedilol and its underlying mechanisms in a mouse model of acrylamide-induced brain injury. Materials and Methods: Mice were treated with acrylamide (50 mg/kg/day, IP) and carvedilol (5 and 10 mg/kg/day, oral) for 11 continuous days. At the end of the experiment, mice were subjected to gait assessment. They were sacrificed and brain tissues were collected for histological and biochemical analysis. Results: The results showed that treatment of mice with carvedilol decreased acrylamide-induced bodyweight loss, abnormal gait, and histopathological damage in the brain tissue. Carvedilol treatment significantly reduced the levels of malondialdehyde (MDA) and carbonyl protein and increased the levels of glutathione (GSH), catalase, superoxide dismutase (SOD), nuclear factor erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1). Carvedilol treatment also decreased myeloperoxidase (MPO) activity, expression of nuclear factor kappa B (NF-κB), inducible nitric oxide synthase (iNOS), overproduction of nitric oxide (NO) and proinflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in the brain of mice exposed to acrylamide. Furthermore, administration of carvedilol significantly decreased the levels of bax, cytochrome-c, and caspase-3 as markers of apoptosis in acrylamide-treated mice. Conclusion: These findings indicate that carvedilol is able to attenuate acrylamide-induced damage to the CNS by inhibition of oxidative stress, inflammation, and apoptosis. }, keywords = {Acrylamide,Apoptosis,Brain damage,Carvedilol,Inflammation,Oxidative stress}, url = {https://ijbms.mums.ac.ir/article_19400.html}, eprint = {https://ijbms.mums.ac.ir/article_19400_6fc5aef955bed352f40f28b5f35a166c.pdf} } @article { author = {Xu, Jing and Wang, Shujuan and Bu, Shanshan and Guo, Xiaoqi and Ge, Hong}, title = {Theaflavin promoted apoptosis in nasopharyngeal carcinoma unexpectedly via inducing autophagy in vitro}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {68-74}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.59190.13143}, abstract = {Objective(s): This study aimed to investigate the mechanism of the anticancer effect of theaflavin (TF) in nasopharyngeal carcinoma.Materials and Methods: CNE2 cells were used to study the anticancer effect of TF. This study used Cell Counting Kit-8 (CCK8) assay on proliferation and used flow cytometry to detect apoptosis. The protein expression of Bcl-2, Bax, caspase 3, and caspase 9 was detected by Western blot, and autophagy-related proteins were also detected.Results: TF inhibited proliferation of CNE2 cells, promoted apoptosis, and up-regulated the expression of caspase 3, caspase 9, and Bax, and decreased the level of Bcl-2. Unexpectedly, TF induced autophagy rather than inhibiting autophagy through up-regulating the levels of the autophagy marker light chain 3 (LC3) and Lysosomal-associated membrane protein 1 (LAMP1) and reducing levels of the autophagosome cargo protein p62, and the effect was via the mTOR pathway. Besides, autophagy inhibitor Chloroquine (CQ) suppressed the effect of TF on Bax, Bcl-2 and activation of caspase 3 and caspase 9.Conclusion: TF promoted apoptosis of nasopharyngeal carcinoma cells, the mechanism was unexpectedly involved in inducing autophagy.}, keywords = {Apoptosis,Autophagy,Nasopharyngeal carcinoma,Proliferation,Theaflavin}, url = {https://ijbms.mums.ac.ir/article_19399.html}, eprint = {https://ijbms.mums.ac.ir/article_19399_5f49498cdcb359725be7ce581f3b90f8.pdf} } @article { author = {Mahdi, Parvane and Pourbakht, Akram and Yazdi, Alireza and Anari, Mahtab and Mahabadi, Vahid and Kamali, Mohammad}, title = {Metabotropic glutamate receptor: A new possible therapeutic target for cochlear synaptopathy}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {75-83}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.59970.13296}, abstract = {Objective(s): Cochlear synaptopathy is a common cause of auditory disorders in which glutamate over-activation occurs. Modulating glutamatergic pathways has been proposed to down-regulate post-synaptic excitation.Materials and Methods: 12-guinea pigs as  sham and test groups were exposed to a 4-kHz noise at 104 dB SPL, for 2 hr. Pre-exposure intra-tympanic injection with LY354740 and normal saline 9% was applied in the test and sham groups. The amplitude growth of ABR-wave-I and wave-III latency shift with noise were considered in pre- and post-exposure times. The synapses were observed by transmission electron-microscopy.Results: ABR thresholds recovered 1-week post-exposure in both groups. The reduction of wave-I amplitude at 4, 6, and 8 kHz were statistically different between pre- and 1- day post-exposure and recovered mostly in the sham group. The amount of latency shift in masked ABR was different between pre- and all post-exposure, and the response could not be detected at higher than 50 dB SL noise. However, the response detectability increased to 60 dB SL noise, and the significance of differences between pre- and post-exposure persisted only at the high level of noise in the test group. In electron-microscopy of sham samples, the size of the ribbon was larger, spherical with an irregularity, and hollow. The post-synaptic density was thicker and missed its flat orientation.Conclusion: The higher slope of the ABR-wave I amplitude, the more tolerance of noise in masked ABR, concomitant with the histological finding that revealed less synaptic damage, confirmed the therapeutic effect of LY354740 in cochlear synaptopathy.}, keywords = {Cochlear synaptopathy,Excitotoxicity,Glutamate,Hidden hearing loss,Noise-induced hearing loss}, url = {https://ijbms.mums.ac.ir/article_19350.html}, eprint = {https://ijbms.mums.ac.ir/article_19350_4b07c8a037577d45573db88c22180aa3.pdf} } @article { author = {Jiang, Hong and Zhang, Suying}, title = {Therapeutic effect of acute and chronic use of different doses of vitamin D3 on seizure responses and cognitive impairments induced by pentylenetetrazole in immature male rats}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {84-95}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.60123.13328}, abstract = {Objective(s): This study aimed to evaluate the effects of acute and chronic intake of different doses of vitamin D3 on seizure responses and cognitive impairment induced by pentylenetetrazole (PTZ) in immature male rats.Materials and Methods: Sixty-six immature male NMRI rats were divided into control (10), epileptic (10), and treatment groups (46). The stage 5 latency (S5L) and stage 5 duration (S5D) were assessed along with the shuttle box test. Levels of antioxidant enzymes and inflammatory factors along with genes involved in inflammation, oxidative damage, apoptosis, and mTORc1 were measured in the hippocampus tissue of the brain of controlled and treated rats. Serum levels of parathyroid hormone (PTH), vitamin D, calcium, and phosphorus were also assessed.Results: The results showed that the ability to learn, memory consolidation, and memory retention in epileptic rats were reduced. In addition, S5D increased and S5L decreased in epileptic rats, while being effectively ameliorated by chronic and acute vitamin D intake. The results showed that vitamin D in different doses acutely and chronically decreased the levels of oxidative and inflammatory biomarkers in hippocampus tissue and inhibited the expression of genes involved in inflammation, oxidative damage, apoptosis, and mTORc1 in the hippocampus tissue of epileptic rats. Conclusion: The results showed that vitamin D in different doses acutely and chronically could improve cognitive impairments and convulsive responses in epileptic rats by improving neurotransmission, inflammation, apoptosis, and oxidative damage.}, keywords = {Apoptosis,Epilepsy,GABA receptor,Inflammation,NMDA receptor,Vitamin D3}, url = {https://ijbms.mums.ac.ir/article_19398.html}, eprint = {https://ijbms.mums.ac.ir/article_19398_4fb8aa02f48237265c5f5125bd12cb11.pdf} } @article { author = {Mirershadi, Fatemeh and Ahmadi, Mahdi and Rahbarghazi, Reza and Heiran, Hossain and Keyhanmanesh, Rana}, title = {C-Kit+ cells can modulate asthmatic condition via differentiation into pneumocyte-like cells and alteration of inflammatory responses via ERK/NF-ƙB pathway}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {96-102}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2021.59946.13293}, abstract = {Objective(s): The exact role of the progenitor cell types in the dynamic healing of asthmatic lungs is lacking. This investigation was proposed to evaluate the effect of intratracheally administered rat bone marrow-derived c-kit+ cells on ovalbumin-induced sensitized male rats.Materials and Methods: Forty rats were randomly divided into 4 groups; healthy rats received phosphate-buffered saline (PBS) (C); sensitized rats received PBS (S); PBS containing C-kitˉ cells (S+C-kit-); and PBS containing C-kit+ cells (S+C-kit+). After two weeks, circulatory CD4+/CD8+ T-cell counts and pulmonary ERK/NF-ƙB signaling pathway as well as the probability of cellular differentiation were assessed. Results: The results showed that transplanted C-Kit+ cells were engrafted into pulmonary tissue and differentiated into epithelial cells. C-Kit+ cells could increase the number of CD4+ cells in comparison with the S group (P<0.001); however, they diminished the level of CD8+ cells (P<0.01). Moreover, data demonstrated increased p-ERK/ERK ratio (P<0.001) and NF-ƙB level (P<0.05) in sensitized rats compared with the C group. The administration of C-kit+, but not C-Kit-, decreased p-ERK/ERK ratio and NF-ƙB level compared with those of the S group (P<0.05). Conclusion: The study revealed that C-Kit+ cells engrafted into pulmonary tissue reduced the NF-ƙB protein level and diminished p-ERK/ERK ratio, leading to suppression of inflammatory response in asthmatic lungs. }, keywords = {Asthma,C-kit cells,CD4+/CD8+,Differentiation,NF-ƙB,p-ERK/ERK}, url = {https://ijbms.mums.ac.ir/article_19285.html}, eprint = {https://ijbms.mums.ac.ir/article_19285_23a073496c5f157c1afb8c07b2f3c76a.pdf} } @article { author = {Yu, Yani and Dong, Hui and Sun, Jingyi and Li, Baoshuang and Chen, Yueqi and Feng, Moxuan and Yang, Xiaoqian and Jiang, Wei}, title = {Hepatitis B virus X mediates podocyte pyroptosis by regulating the ROS/NLRP3 signaling pathway in hepatitis B virus-associated glomerulonephritis}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {103-109}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2022.61105.13520}, abstract = {Objective(s): This study was designed to investigate whether HBx-induced podocyte injury is related to the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome and the specific mechanism of the oxidative stress pathway in hepatitis B virus-associated glomerulonephritis (HBV-GN).Materials and Methods: The HBx gene was overexpressed in renal podocytes to mimic HBV-GN. Podocyte morphology was observed under a scanning electron microscope. Reactive oxygen species (ROS) generation was detected by dichlorodihydrofluorescein diacetate (DCFH-DA) assay. The podocytes in each group were treated with Hoechst 33342 and subjected to immunofluorescence staining. Caspase-1 activity and LDH levels were assessed with a Caspase-1 Activity Assay Kit and an LDH ELISA Kit, respectively. The expression of all pyroptosis-related proteins was examined by Western blot analysis.Results: Pyroptosis-related proteins, including NLRP3, apoptosis-associated speck-like protein containing card (ASC), caspase-1, IL-1β, and IL-18 (P<0.05), were up-regulated upon HBx overexpression, and caspase-1 enzyme activity and LDH and Desmin expression were also enhanced (P<0.05). NLRP3 knockdown attenuated the increased expression of pyroptosis-related proteins upon HBx overexpression (P<0.05), which was also achieved by the addition of an ROS inhibitor (P<0.05).Conclusion: HBx regulates podocyte pyroptosis in HBV-GN by targeting the NLRP3 inflammasome, and mitochondrial oxidative stress plays an important role in this process.}, keywords = {Glomerulonephritis,HBx,NLRP3,Pyroptosis,ROS}, url = {https://ijbms.mums.ac.ir/article_19488.html}, eprint = {https://ijbms.mums.ac.ir/article_19488_92687f9c59c49971b7d4f4f034823b31.pdf} } @article { author = {Shaaban, Zahra and Tamadon, Amin and Jafarzadeh Shirazi, Mohammad Reza and Zamiri, Mohammad Javad and Derakhshanfar, Amin}, title = {Maternal aromatase inhibition via letrozole altered RFamide-related peptide-3 and gonadotropin-releasing hormone expression in pubertal female rats}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {110-120}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2022.60962.13499}, abstract = {Objective(s): Despite prevalence of polycystic ovary syndrome (PCOS) among childbearing women and development of many animal models for this syndrome, information on its etiology is still scarce. The intrauterine hyperandrogenic environment may underlie changes at the level of hypothalamus, pituitary, ovary organization in female offspring, and PCOS later in life. Letrozole has been shown to mimic reproductive and metabolic characteristics of PCOS in adult rodent models. Therefore, this research aimed to assess the condition in a prenatal letrozole-treated rat model. Materials and Methods: Twenty-eight female rats dams receiving letrozole at certain doses during late pregnancy were used in the trial.  Pregnant Sprague-Dawley rats (n=21) received letrozole treatment on gestation days 16–18 at doses of 1.25, 1.0, 0.75, 0.5, and 0.25 mg/kg body weight (BW).    Results: Prenatal letrozole treatment delayed parturition time and reduced the litter size in pregnant dams (P<0.0001). Late puberty onset, irregular ovarian cyclicity, increased anogenital distance (AGD), body weight gain, serum testosterone concentration, and reduced estradiol levels (P<0.0001) were observed in the female offspring of dams receiving 1.25 and 1 mg/kg BW letrozole. Furthermore, letrozole at 1.25 and 1 mg/kg BW showed increased RFRP and decreased GnRH mRNA expression (P<0.0001). Letrozole treatment at doses of 1 mg/kg BW and lower was not fetotoxic. Conclusion: It was concluded that 1 mg/kg BW letrozole may be suggested for prenatal PCOS induction. }, keywords = {Gonadotropin-Releasing Hormone,Hypothalamus,Letrozole,Polycystic ovary syndrome Prenatal,Rat,RFamide-related peptide-3}, url = {https://ijbms.mums.ac.ir/article_19500.html}, eprint = {https://ijbms.mums.ac.ir/article_19500_37d3362a509f1dbdd6b8d309166e8c73.pdf} } @article { author = {Aydemir, Fuat and Ulku, Cagatay Han and Elmas, Cigdem and Seymen, Cemile Merve}, title = {Analysis of potential protective effects of caffeic acid phenethyl ester against gentamicin ototoxicity: An experimental study}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {121-125}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2022.60794.13467}, abstract = {Objective(s): In this study, it is aimed to investigate the potential protective effect of caffeic acid phenethyl ester (CAPE) on ototoxicity caused by gentamicin in a rat model.Materials and Methods: Thirty Wistar albino rats were divided into 3 groups. Group I was selected as the control group. Gentamicin was administered intraperitoneally in group II, gentamicin and CAPE in group III. Audiological assessment was performed by the distortion product otoacoustic emission (DPOAE) and auditory brainstem response (ABR) measurements before and after treatment of each group. At the end of the study all rats were decapitated, cochlea was removed and electron microscopic examination was performed. Results: In group II post-treatment DPOAE levels were found to be lower than pretreatment DPOAE levels (P<0.05). However, in group III, there is no significant difference between pre- and post-treatment DPOAE levels (P>0.05). Except for Group I, ABR thresholds increased after the procedure and this increase was statistically significant (P<0.0001). According to histological examination by transmission electron microscopy, CAPE has a cellular protective effect against gentamicin ototoxicity. Conclusion: CAPE may ameliorate hearing deterioration caused by gentamicin ototoxicity and protect the cochlear cells from apoptosis due to the strong antioxidant effect.}, keywords = {Aminoglycoside,Anti-oxidant,caffeic acid phenethyl ester,Gentamicin,Ototoxicity}, url = {https://ijbms.mums.ac.ir/article_19469.html}, eprint = {https://ijbms.mums.ac.ir/article_19469_3fa003175c4d144fc4a18c71c65b313e.pdf} } @article { author = {Bayat, Gholamreza and Hashemi, Seyed Ali and Karim, Hosein and Fallah, Parviz and Hedayatyanfard, Keshvad and Bayat, Mahnaz and Khalili, Azadeh}, title = {Biliary cirrhosis-induced cardiac abnormality in rats: Interaction between Farnesoid-X-activated receptors and the cardiac uncoupling proteins 2 and 3}, journal = {Iranian Journal of Basic Medical Sciences}, volume = {25}, number = {1}, pages = {126-133}, year = {2022}, publisher = {Mashhad University of Medical Sciences}, issn = {2008-3866}, eissn = {2008-3874}, doi = {10.22038/ijbms.2022.60888.13485}, abstract = {Objective(s): This study aimed to evaluate the relationship between Farnesoid-X-activated receptors (FXR) as nuclear regulators of the antioxidant defense system as well as cardiac mitochondrial carrier proteins of UCP2 and UCP3 in cardiac damage induced by cirrhosis. Materials and Methods: Twenty-two male Wistar rats (200–250 g) were randomly divided into 3 experimental groups, including a control group (n=6), a sham-operated group (n=8), and a bile duct ligated (BDL) group (n=8). Four weeks after surgical intervention, biochemical assessment (AST, ALT, GGT, LDH, and ALP), histological observation, and molecular evaluation (FXR, UCP2, UCP3, BNP, Caspase3, and GAPDH) using real-time RT-PCR were performed. Results: Compared with the sham-operation group, the BDL group showed a significant rise in liver enzymes of AST, ALT, GGT, LDH, and ALP. Defined fibrotic and necrotic bundles and thick reticulin fibers were also found in BDL liver tissue. Besides liver morphological alterations, left ventricles of BDL ones were also associated with defined cardiomyocyte hypertrophy, myofiber vacuolization, and clear pigmentation. Findings showed a significant up-regulation of cardiac Brain Natriuretic Peptide (BNP) along with marked down-regulation in hepatic FXR, cardiac FXR, and cardiac UCP2 and UCP3. However, the expression of caspase 3 in the cardiac tissue was not affected by BDL operation during 4 weeks. Conclusion: Expression of FXR as an upstream regulator of cellular redox status, besides the non-enzymatic ROS buffering defense system of cardiac UCPs, has a pivotal role in the pathogenesis of cirrhotic-induced cardiac abnormality in rats.}, keywords = {Cardiomyopathy,cholestasis,Farnesoid-X-receptor,Liver Cirrhosis,Mitochondrial uncoupling proteins}, url = {https://ijbms.mums.ac.ir/article_19499.html}, eprint = {https://ijbms.mums.ac.ir/article_19499_c68621b1f16a2e3808af654c208eb07b.pdf} }