Iranian Journal of Basic Medical Sciences最新文献

{"title":"Antiarrhythmic potentials of irisin in ischemia/reperfusion injury of diabetic rats through modulating mitochondria-endoplasmic reticulum interaction and inhibiting pyroptosis.","authors":"Xiaona Zhang Zhang, Kai Jing, Wei Ma, Jin Wang","doi":"10.22038/ijbms.2024.78069.16878","DOIUrl":"10.22038/ijbms.2024.78069.16878","url":null,"abstract":"<p><strong>Objectives: </strong>Myocardial arrhythmia is a major complication of ischemia-reperfusion (I/R) injury in patients with diabetes. Irisin has significant cardioprotective effects, while its role in the pathophysiology of I/R injury-induced myocardial arrhythmia in the presence of diabetes is not well identified. Here, we aimed to investigate the potential antiarrhythmic impacts and mechanisms (mitochondrial biogenesis, endoplasmic reticulum (ER) stress, and pyroptosis) by which irisin reduces I/R injury-induced myocardial arrhythmia in diabetic rats.</p><p><strong>Materials and methods: </strong>Thirty high-fat diet-induced diabetic rats were subjected to I/R injury and myocardial arrhythmia. Irisin (0.5 μg/kg/day) was injected intraperitoneally before induction of I/R injury. Electrocardiography was used to measure the incidence and severity of ventricular arrhythmias. ELISA and western blotting analyses were employed to quantify the expression of mitochondrial biogenesis, ER stress, and pyroptosis-related proteins in ischemic myocardium.</p><p><strong>Results: </strong>Irisin treatment in diabetic rats significantly decreased the lactate dehydrogenase level and the number and severity of arrhythmia induced by I/R injury. Irisin up-regulated the expression of mitochondrial biogenesis-related proteins while down-regulating the expression of ER stress and pyroptosis-related proteins. Furthermore, the inhibition of mitochondrial quality control by mdivi-1 significantly abolished the cardioprotective effect of irisin.</p><p><strong>Conclusion: </strong>Our findings suggest that irisin reduced myocardial arrhythmia induced by I/R injury in diabetic rats by modulating the interaction of mitochondrial biogenesis and ER stress proteins and inhibiting the pyroptosis pathway. These findings provide a promising strategy for managing myocardial arrhythmia in diabetic patients, but supplementary studies are needed to confirm the clinical efficacy of irisin in these patients.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 11","pages":"1440-1446"},"PeriodicalIF":2.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11459340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"C-71980262, a novel small molecule against human papilloma virus-16 E6 (HPV-16 E6) with anticancer potency against cervical cancer: A computational guided <i>in vitro</i> approach.","authors":"Ashish Kumar","doi":"10.22038/ijbms.2024.78090.16882","DOIUrl":"10.22038/ijbms.2024.78090.16882","url":null,"abstract":"<p><strong>Objectives: </strong>Human papillomavirus-16 E6 (HPV-16 E6) forms a heterodimer complex to up-regulate the degradation of tumor suppressor protein p53 to promote cervical cancer. This study aims to identify a novel small molecule against E6 with anticancer efficacy against HPV-16, a prime high-risk serotype inducer for cervical cancer.</p><p><strong>Materials and methods: </strong>Autodock-vina-based high-throughput virtual screening and atomistic molecular dynamic simulations were used for identification of targeted lead molecules. HPV-16 infected SiHa and CaSki cell lines were used to validate the lead compound in vitro. Proliferation of cancer cells was analyzed by MTT assay and flow cytometry was used to analyze target inhibition, apoptosis, and p53.</p><p><strong>Results: </strong>High throughput virtual screening and molecular dynamic simulation identified C-71980262 as a lead candidate that could bind HPV-E6. Atomistic molecular dynamic simulation of E6 bound C-71980262 for 200 ns showed that the predicted ligand binding was stable with minimal energy expenditure, proposing the viability and veracity of the assessed molecule. C-71980262 inhibited the proliferation of SiHa and CaSki cells with GI50 values of 355.70 nM and 505.90 nM, respectively. The compound reduced HPV-16 E6 while inducing early and late-phase apoptosis in these cells. Treatment with C-71980262 increased the p53-positive populations in SiHa and CaSki cells.</p><p><strong>Conclusion: </strong>C-71980262 was identified as a novel lead molecule that could inhibit the HPV-16 E6 and increase p53 in cervical cancer cells. Further in vitro and in vivo validation is warranted to consolidate and corroborate this lead compound against HPV-induced cancer progression.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 11","pages":"1389-1396"},"PeriodicalIF":2.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11459339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Introduction of <i>LPIN1</i> as a potential diagnostic and prognostic biomarker for gastric cancer via integrative bioinformatics analysis of a competing endogenous RNA network and experimental validation.","authors":"Milad Daneshmand-Parsa, Parvaneh Nikpour","doi":"10.22038/ijbms.2024.74686.16216","DOIUrl":"10.22038/ijbms.2024.74686.16216","url":null,"abstract":"<p><strong>Objectives: </strong>Identification of effective biomarkers is crucial for the heterogeneous disease of gastric cancer (GC). Recent studies have focused on the role of pseudogenes regulating gene expression through competing endogenous RNA (ceRNA) networks, however, the pseudogene-associated ceRNA networks in GC remain largely unknown. The current study aimed to construct and analyze a three-component ceRNA network in GC and experimentally validate a ceRNA.</p><p><strong>Materials and methods: </strong>A comprehensive analysis was conducted on the RNA-seq and miRNA-seq data of The Cancer Genome Atlas (TCGA) stomach adenocarcinoma (STAD) dataset to identify differentially-expressed mRNAs (DEMs), pseudogenes (DEPs), and miRNAs (DEMis). Pseudogene-associated ceRNA and protein-protein interaction (PPI) networks were constructed, and functional enrichment analyses were performed. DEMs and DEPs with degree centralities≥2 were selected for survival analysis. A ceRNA was further selected for experimental validation.</p><p><strong>Results: </strong>10,145 DEMs, 3576 DEPs, and 66 DEMis were retrieved and a ceRNA network was then constructed by including DEMis with concurrent interactions with at least a DEM and a DEP. Functional enrichment analysis demonstrated that DEMs of the ceRNA network were significantly enriched in cancer-associated pathways. <i>LPIN1</i> and <i>WBP1L</i> were two mRNAs showing an association with STAD patients overall survival. Expression analysis of <i>LPIN1</i> showed a significant decrease in GC tumors compared to non-tumor tissues (<i>P</i>=0.003).</p><p><strong>Conclusion: </strong>Our research emphasizes the significant implications of ceRNA networks in the development of new biomarkers for the detection and prognosis of cancer. Further examination is necessary to explore the functional roles of <i>LPIN1</i> in the pathogenesis of GC.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 11","pages":"1456-1463"},"PeriodicalIF":2.1,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11459342/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142390531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin improves memory via AMPK/mTOR-dependent route in a rat model of Alzheimer's disease.","authors":"Reza Ale Mahmoud Mehraban, Parvin Babaei, Kambiz Rohampour, Adele Jafari, Zoleikha Golipoor","doi":"10.22038/IJBMS.2023.73075.15879","DOIUrl":"10.22038/IJBMS.2023.73075.15879","url":null,"abstract":"<p><strong>Objectives: </strong>Metformin, as an insulin sensitizer, is a familiar antidiabetic drug. Increasing evidence points to metformin's protective effects against Alzheimer's disease (AD). However, the mechanism is not well understood. The present study evaluated whether inhibiting AMPK and activating mTOR could stop metformin from improving memory in rats with streptozotocin (STZ) -induced Alzheimer's disease.</p><p><strong>Materials and methods: </strong>Twelve-week-old Wistar rats, were injected 3 mg/kg STZ intracerebroventricularly on days 1 and 3 to develop the animal model. Metformin was applied orally at 100 mg/kg (17 days). Forty-five min before the retrieval phase, dorsomorphin (DM; AMPK inhibitor, 2 M) and MHY (mTOR activator, 0.1 M) were administered. Morris Water Maze (MWM) and shuttle box were utilized to measure spatial and passive avoidance memory, respectively. Congo red staining was used to identify cortical amyloid deposition.</p><p><strong>Results: </strong>The findings exhibited a considerable enhancement in spatial learning and memory in the metformin treatment group (<i>P</i>≤0.05). Injection of DM and MHY alone could not significantly change MWM and passive avoidance. Additionally, co-administration of DM and MHY increased escape latency (<i>P</i>≤0.001) and reduced the total time spent in the target quadrant (TTS) (<i>P</i>≤0.05) compared to the STZ+MET group during retrieval of MWM. Also, co-injection of DM and MHY increased step-through latency (STL) and decreased time spent in the dark compartment (TDC) compared to the STZ+MET group (<i>P</i>≤0.001).</p><p><strong>Conclusion: </strong>Metformin appears to have a therapeutic impact by activating AMPK and inactivating mTOR. As a result, it could be used as an Alzheimer's treatment strategy.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 3","pages":"360-365"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10849203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139706741","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Melatonin enhanced the cardioprotective effects of HTK solution on Langendorff-perfused mouse hearts subjected to ischemia/reperfusion.","authors":"Mingchu Sun, Zihui Zhang, Yue Yin, Lu Yu, Wenhua Jiang, Chan Zhang, Chunhu Gu, Heng Ma, Yishi Wang","doi":"10.22038/IJBMS.2023.74152.16109","DOIUrl":"10.22038/IJBMS.2023.74152.16109","url":null,"abstract":"<p><strong>Objectives: </strong>Cardiac arrest is a crucial procedure in various cardiac surgeries, during which the heart is subjected to an ischemic state. The occurrence of ischemia/reperfusion (I/R) injury is inevitable due to aortic blockage and opening. The Histidine-tryptophan-ketoglutarate (HTK) solution is commonly used as an organ protection liquid to mitigate cardiac injury during cardiac surgery. Despite its widespread use, there is significant potential for improving its protective efficacy.</p><p><strong>Materials and methods: </strong>The cardioprotective effect of HTK solution with and without melatonin was evaluated using the isolated Langendorff-perfused mouse heart model. The isolated C57bL/6 mouse hearts were randomly divided into four groups: control, I/R, HTK solution treatment before reperfusion (HTK+I/R), and HTK solution combined with melatonin before reperfusion (HTK+M+I/R). Cardiac function and myocardial injury markers were then measured. AMP-activated protein kinase α2 (AMPKα2) KO mice were used to investigate the underlying mechanism.</p><p><strong>Results: </strong>In our study, we found that melatonin significantly improved the protective effects of HTK solution in an isolated Langendorff-perfused mouse model, mechanistically by reducing mitochondrial damage, improving energy metabolism, inhibiting cardiomyocyte apoptosis, and reducing myocardial infarction size. We also observed that the HTK solution alone was ineffective in inhibiting ER stress, but when melatonin was added, there was a significant reduction in ER stress. Furthermore, melatonin was found to alleviate carbonyl stress during cardiac I/R. Interestingly, our results showed that the cardioprotective properties of melatonin were dependent on AMPKα2.</p><p><strong>Conclusion: </strong>The findings presented in this study offer a valuable empirical foundation for the development of perioperative cardioprotective strategies.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 3","pages":"366-374"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10849209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139706772","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fucoidan alleviated autoimmune diabetes in NOD mice by regulating pancreatic autophagy through the AMPK/mTOR1/TFEB pathway.","authors":"Haiqi Gao, Yifan Zhou, Chundong Yu, Guifa Wang, Wenwei Song, Zixu Zhang, Lu Lu, Meilan Xue, Hui Liang","doi":"10.22038/IJBMS.2023.68739.14981","DOIUrl":"10.22038/IJBMS.2023.68739.14981","url":null,"abstract":"<p><strong>Objectives: </strong>The present study investigated the effect and its underlying mechanisms of fucoidan on Type 1 diabetes mellitus (T1DM) in non-obese diabetic (NOD) mice.</p><p><strong>Materials and methods: </strong>Twenty 7-week-old NOD mice were used in this study, and randomly divided into two groups (10 mice in each group): the control group and the fucoidan treatment group (600 mg/kg. body weight). The weight gain, glucose tolerance, and fasting blood glucose level in NOD mice were detected to assess the development of diabetes. The intervention lasted for 5 weeks. The proportions of Th1/Th2 cells from spleen tissues were tested to determine the anti-inflammatory effect of fucoidan. Western blot was performed to investigate the expression levels of apoptotic markers and autophagic markers. Apoptotic cell staining was visualized through TdT-mediated dUTP nick-end labeling (TUNEL).</p><p><strong>Results: </strong>The results suggested that fucoidan ameliorated T1DM, as evidenced by increased body weight and improved glycemic control of NOD mice. Fucoidan down-regulated the Th1/Th2 cells ratio and decreased Th1 type pro-inflammatory cytokines' level. Fucoidan enhanced the mitochondrial autophagy level of pancreatic cells and increased the expressions of Beclin-1 and LC3B II/LC3B I. The expression of p-AMPK was up-regulated and p-mTOR1 was inhibited, which promoted the nucleation of transcription factor EB (TFEB), leading to autophagy. Moreover, fucoidan induced apoptosis of pancreatic tissue cells. The levels of cleaved caspase-9, cleaved caspase-3, and Bax were up-regulated after fucoidan treatment.</p><p><strong>Conclusion: </strong>Fucoidan could maintain pancreatic homeostasis and restore immune disorder through enhancing autophagy via the AMPK/mTOR1/TFEB pathway in pancreatic cells.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 1","pages":"31-38"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10722478/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139074070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Joining COPE: Opportunities and benefits for the Iranian Journal of Basic Medical Sciences.","authors":"Leila Arabi, Ali Roohbakhsh, Bizhan Malaekeh-Nikouei, Bibi Sedigheh Fazly Bazzaz","doi":"10.22038/ijbms.2023.76381.16530","DOIUrl":"10.22038/ijbms.2023.76381.16530","url":null,"abstract":"","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 1","pages":"1-2"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10722480/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139074073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Voluntary exercise improves pulmonary inflammation through NF-κB and Nrf2 in type 2 diabetic male rats.","authors":"Seyed Zanyar Athari, Fariba Mirzaei Bavil, Rana Keyhanmanesh, Hajie Lotfi, Yousef Sajed, Aref Delkhosh, Fariba Ghiasi","doi":"10.22038/IJBMS.2023.70416.15307","DOIUrl":"10.22038/IJBMS.2023.70416.15307","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to evaluate the effects of voluntary exercise as an anti-inflammatory intervention on the pulmonary levels of inflammatory cytokines in type 2 diabetic male rats.</p><p><strong>Materials and methods: </strong>Twenty-eight male Wistar rats were divided into four groups (n=7), including control (Col), diabetic (Dia), voluntary exercise (Exe), and diabetic with voluntary exercise (Dia+Exe). Diabetes was induced by a high-fat diet (4 weeks) and intraperitoneal injection of streptozotocin (35 mg/kg), and animals did training on the running wheel for 10 weeks as voluntary exercise. Finally, the rats were euthanized and the lung tissues were sampled for the evaluation of the levels of pulmonary interleukin (IL)-10, IL-11, and TNF-α using ELISA, and the protein levels of Nrf-2 and NF-κB using western blotting and tissue histopathological analysis.</p><p><strong>Results: </strong>Diabetes reduced the IL-10, IL-11, and Nrf2 levels (<i>P</i><0.001 to P<0.01) and increased the levels of TNF-α and NF-κB compared to the Col group (<i>P</i><0.001). Lung tissue levels of IL-10, IL-11, and Nrf2 in the Dia+Exe group enhanced compared to the Dia group (<i>P</i><0.001 to <i>P</i><0.05), however; the TNF-α and NF-κB levels decreased (<i>P</i><0.001). The level of pulmonary Nrf2 in the Dia+Exe group was lower than that of the Exe group while the NF-κB level increased (<i>P</i><0.001). Moreover, diabetes caused histopathological changes in lung tissue which improved with exercise in the Dia+Exe group.</p><p><strong>Conclusion: </strong>These findings showed that voluntary exercise could improve diabetes-induced pulmonary complications by ameliorating inflammatory conditions.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 1","pages":"74-80"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10722479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139074076","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of zingerone on rat induced testicular toxicity by sodium arsenite via oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, and autophagy pathways.","authors":"Sibel Çiğdem Tuncer, Cihan Gur, Sefa Kucukler, Serkan Ali Akarsu, Fatih Mehmet Kandemir","doi":"10.22038/IJBMS.2024.73342.15934","DOIUrl":"https://doi.org/10.22038/IJBMS.2024.73342.15934","url":null,"abstract":"<p><strong>Objectives: </strong>This study aimed to investigate the effects of zingerone (ZNG) treatment on testicular toxicity in rats induced by sodium arsenite (SA).</p><p><strong>Materials and methods: </strong>In the study, five groups were formed (n=7) and the experimental groups were designated as follows; Vehicle group, ZNG group, SA group, SA+ZNG 25 group, and SA+ZNG 50 group. While SA was administered orally to rats at 10 mg/kg/bw, ZNG was given to rats orally at 25 and 50 mg/kg/bw doses for 14 days.</p><p><strong>Results: </strong>As a result of the presented study, an increase was observed in the MDA contents of the testicular tissue of the rats administered SA, while significant decreases were observed in GSH levels, SOD, CAT, and GPx activities. The mRNA transcript levels of the pro-inflammatory genes NF-κB, TNF-α, IL-1β, and IL-6 were triggered after SA administration. Additionally, SA administration caused inflammation by increasing RAGE, NLRP3, and JAK-2/STAT3 gene expression. Moreover, endoplasmic reticulum (ER) stress occurred in the testicular tissues of SA-treated rats and thus ATF-6, PERK, IRE1, and GRP78 genes were up-regulated. SA caused apoptosis by up-regulating Bax and Caspase-3 expressions and inhibiting Bcl-2 expression in testicles. SA caused histological irregularities in the testicles, resulting in decreased sperm quality.</p><p><strong>Conclusion: </strong>ZNG treatment reduced SA-induced oxidative stress, ER stress, inflammation, apoptosis, and histological irregularities in the testicles while increasing sperm quality. As a result, it was observed that ZNG could alleviate the toxicity caused by SA in the testicles.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 5","pages":"603-610"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11017849/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140848897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of electroacupuncture combined with sulforaphane in the treatment of sarcopenia in SAMP8 mice.","authors":"Fei Guo, Linlin Fu, Zhenchan Lu","doi":"10.22038/IJBMS.2024.71345.15509","DOIUrl":"https://doi.org/10.22038/IJBMS.2024.71345.15509","url":null,"abstract":"<p><strong>Objectives: </strong>Skeletal muscles mitochondrial dysfunction is the main cause of sarcopenia. Both electroacupuncture (EA) and sulforaphane (SFN) have been shown to improve oxidative stress and inflammation levels to maintain mitochondrial function, but the effects and mechanisms of their combination on sarcopenia are unclear. This study aimed to investigate the regulatory effects of EA combined with SFN on sarcopenia.</p><p><strong>Materials and methods: </strong>SAMP8 mice were used and intervened with EA or SFN, respectively, and Masson and HE staining were used to observe pathological changes in skeletal muscle tissue. Transmission electron microscopy was used to detect tissue mitochondrial changes. TUNEL staining was used to assess apoptosis. The biochemical and molecular content was tested by ELISA, western blot, and qRT-PCR.</p><p><strong>Results: </strong>The results showed that oxidative stress, apoptosis, and IL-6, TNF-α, Atrogin-1, and MuRF1 levels in skeletal muscles cells were suppressed and mitochondrial damage was repaired after EA or SFN intervention. In addition, we found that the above changes were associated with the activation of the AMPK/Sirt1/PGC-1α pathway in skeletal muscle tissues, and the promotion effect of combined EA and SFN intervention was more significant.</p><p><strong>Conclusion: </strong>In conclusion, this study found that EA combined with SFN mediated the repair of mitochondrial damage through activation of the AMPK/Sirt1/PGC-1α pathway, thereby alleviating skeletal muscles morphology and function in sarcopenia. This study combines EA with SFN, which not only broadens the use of electroacupuncture and SFN but also provides a scientific experimental basis for the treatment of sarcopenia.</p>","PeriodicalId":14495,"journal":{"name":"Iranian Journal of Basic Medical Sciences","volume":"27 5","pages":"560-566"},"PeriodicalIF":2.2,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11017848/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140858936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}