Archives of Physiology and Biochemistry最新文献

{"title":"Aerobic training increases renal antioxidant defence and reduces angiotensin II levels, mitigating the high mortality in SHR-STZ model.","authors":"Vinicius Guzzoni, Isabel Cristina Mallosto Emerich de Abreu, Mariane Bertagnolli, Roberta Hack Mendes, Adriane Belló-Klein, Dulce Elena Casarini, Karin Flues, Geórgia Orsi Cândido, Janaína Paulini, Kátia De Angelis, Fernanda Klein Marcondes, Maria Cláudia Irigoyen, Tatiana Sousa Cunha","doi":"10.1080/13813455.2024.2377381","DOIUrl":"10.1080/13813455.2024.2377381","url":null,"abstract":"<p><strong>Objectve: </strong>The purpose of the research was to investigate the effects of aerobic training on renal function, oxidative stress, intrarenal renin-angiotensin system, and mortality of hypertensive and diabetic (SHR-STZ) rats.</p><p><strong>Materials and methods: </strong>Blood pressure, creatinine, urea levels, urinary glucose, urine volume, and protein excretion were reduced in trained SHR-STZ rats.</p><p><strong>Results: </strong>Aerobic training not only attenuated oxidative stress but also elevated the activity of antioxidant enzymes in the kid'ney of SHR-STZ rats. Training increased intrarenal levels of angiotensin-converting enzymes (ACE and ACE2) as well as the neprilysin (NEP) activity, along with decreased intrarenal angiotensin II (Ang II) levels. Aerobic training significantly improved the survival of STZ-SHR rats.</p><p><strong>Conclusion: </strong>The protective role of aerobic training was associated with improvements in the renal antioxidative capacity, reduced urinary protein excretion along with reduced intrarenal Ang II and increased NEP activity. These findings might reflect a better survival under the combined pathological conditions, hypertension, and diabetes.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"992-1004"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141625782","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective effects of hyperoxic pre-treatment in human-derived adipose tissue mesenchymal stem cells against in vitro oxidative stress and a rat model of renal ischaemia-reperfusion.","authors":"Shahram Ahmadi Somaghian, Naser Pajouhi, Omid Dezfoulian, Afshin Pirnia, Ayat Kaeidi, Bahram Rasoulian","doi":"10.1080/13813455.2023.2238918","DOIUrl":"10.1080/13813455.2023.2238918","url":null,"abstract":"<p><strong>Objective: </strong>Improvement of cell survival is essential for achieving better clinical outcomes in stem cell therapy. We investigated the effects of hyperoxic pre-treatment (HP) on the viability of human adipose stromal stem cells (ASCs).</p><p><strong>Materials and methods: </strong>MTT and Western blot tests were used to assess cell viability and the expression of apoptosis-related proteins, respectively. For the in-vivo trial, the rats were subjected to renal ischaemia-reperfusion (IR).</p><p><strong>Results: </strong>The results showed that HP could significantly increase the viability of ASCs and decrease apoptotic markers (Bax/BCL-2 ratio and Caspase-3) compared with control cells. There were some additional effects with regard to the improvement of renal structure and function in the animal model. However, the difference between the treated and non-treated transplanted ASCs failed to reach significance.</p><p><strong>Conclusion: </strong>These results suggested that HP could increase the survival of ASCs against oxidative stress-induced damages in the in-vitro condition, but this strategy was not highly effective in renal IR.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"606-615"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9958190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of oxidative stress in diabetes-induced complications and their management with antioxidants.","authors":"Hasandeep Singh, Rajanpreet Singh, Arshdeep Singh, Harshbir Singh, Gurpreet Singh, Sarabjit Kaur, Balbir Singh","doi":"10.1080/13813455.2023.2243651","DOIUrl":"10.1080/13813455.2023.2243651","url":null,"abstract":"<p><p>Diabetes mellitus (DM) is a huge global health issue and one of the most studied diseases, with a large global prevalence. Oxidative stress is a cytotoxic consequence of the excessive development of ROS and suppression of the antioxidant defense system for ROS elimination, which accelerates the progression of diabetes complications such as diabetic neuropathy, retinopathy, and nephropathy. Hyperglycaemia induced oxidative stress causes the activation of seven major pathways implicated in the pathogenesis of diabetic complications. These pathways increase the production of ROS and RNS, which contributes to dysregulated autophagy, gene expression changes, and the development of numerous pro-inflammatory mediators which may eventually lead to diabetic complications. This review will illustrate that oxidative stress plays a vital role in the pathogenesis of diabetic complications, and the use of antioxidants will help to reduce oxidative stress and thus may alleviate diabetic complications.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"616-641"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10351552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leptin Rs7799039 polymorphism is associated with type 2 diabetes mellitus Egyptian patients.","authors":"Amal Ahmed Mohamed, Dina M Abo-Elmatty, Alaa S Wahba, Omnia Ezzat Esmail, Hadeer Saied Mahmoud Salim, Wafaa Salah Mohammed Hegab, Mona Mostafa Farid Ghanem, Nadia Youssef Riad, Doaa Ghaith, Lamiaa I Daker, Shorouk Issa, Noha Hassan Radwan, Eman Sultan, Omar Mohamoud Azzam, Ehab A M El-Shoura","doi":"10.1080/13813455.2023.2265078","DOIUrl":"10.1080/13813455.2023.2265078","url":null,"abstract":"<p><strong>Background: </strong>Leptin (LEP) is an anti-obesity hormone that regulates food intake, energy expenditure, and glucose metabolism. The genetic variants in LEP and the LEP receptor (LEPR) gene may play an important role in the pathogenesis of type 2 diabetes mellitus (T2DM) and obesity. The current study aimed to investigate the association of serum LEP levels, and LEP polymorphisms in LEP (rs7799039, 2548 G/A) with T2DM in Egyptian patients.</p><p><strong>Methods: </strong>A total of 205 subjects were included in the present case-control study, consisting of 100 T2DM patients and 105 healthy controls. The anthropometric, psychometric, and biochemical measurements were taken from all the subjects. The genotyping of LEP gene variants was carried out by polymerase chain reaction TaqMan technology. Serum LEP levels were measured by the ELISA technique.</p><p><strong>Results: </strong>T2DM patients had significantly elevated levels of glycated haemoglobin (HbA1c), fasting blood sugar (FBS), postprandial blood sugar (PPBS), international normalisation ratio (INR), creatinine, urea, cholesterol, triglyceride (TG), and low-density lipoproteins (LDL) and significantly decreased high-density lipoprotein (HDL) compared to healthy subjects. serum LEP levels were significantly decreased <i>p</i> (<0.001) as compared to the control group. LEP gene SNP rs7799039 was associated with an increased diabetic risk with A allele being more frequent in T2DM patients than control subjects. The distribution of the AA genotype and GA genotype of LEP SNP rs7799039 was higher in the diabetic group than control one. In addition, AA + GA genotype carriers had significantly elevated HbA1c, FBS, PPBS, TG, and LDL levels and on the contrary, decreased serum LEP levels compared to GG homozygotes.</p><p><strong>Conclusion: </strong>The genetic polymorphism rs7799039 showed a highly significant correlation with blood LEP. The co-dominant and dominant models of the LEP genetic polymorphism (rs7799039, 2548 G/A) were shown to have a significant correlation with complicated and uncomplicated diabetes individuals, but we have found that serum LEP levels were inversely related with control and diabetes patients. A positive significant association was found between LEP genetic polymorphism (rs7799039, 2548 G/A) and serum LEP in patients and controls. LEP levels and its rs7799039 genetic variant may play a vital role in increasing T2DM susceptibility.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"742-754"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41231912","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A molecular and computational study of galbanic acid as a regulator of Sirtuin1 pathway in inhibiting lipid accumulation in HepG2 cells.","authors":"Hadis Musavi, Hajar Shokri Afra, Farideh Sadeghkhani, Hossein Ghalehnoei, Abbas Khonakdar-Tarsi, Soleiman Mahjoub","doi":"10.1080/13813455.2024.2336911","DOIUrl":"10.1080/13813455.2024.2336911","url":null,"abstract":"<p><strong>Introduction: </strong>Sirtuin1 (SIRT1) plays a crucial role in the pathophysiology of non-alcoholic fatty liver disease. We investigated the mechanistic role of galbanic acid (Gal) as a regulator of SIRT1 <i>in silico</i> and <i>in vitro</i>.</p><p><strong>Methods: </strong>HepG2 cells were treated with Gal in the presence or absence of EX-527, a SIRT1-specific inhibitor, for 24 h. Sirtuin1 gene and protein expression were measured by RT-PCR and Western blotting, respectively. It has been docked to the allosteric reign of SIRT1 (PDB ID: 4ZZJ) to study the effect of Gal on SIRT1, and then the protein and complex molecular dynamic (MD) simulations had been studied in 100 ns.</p><p><strong>Results: </strong>The semi-quantitative results of Oil red (<i>p</i> < .03) and TG level (<i>p</i> < .009) showed a significant reduction in lipid accumulation by treatment with Gal. Also, a significant increase was observed in the gene and protein expression of SIRT1 (<i>p</i> < .05). MD studies have shown that the average root mean square deviation (RMSD) was about 0.51 Å for protein structure and 0.66 Å for the complex. The average of radius of gyration (Rg) is 2.33 and 2.32 Å for protein and complex, respectively, and the pattern of root mean square fluctuation (RMSF) was almost similar.</p><p><strong>Conclusion: </strong>Computational studies show that Gal can be a great candidate to use as a SIRT1 ligand because it does not interfere with the structure of the protein, and other experimental studies showed that Gal treatment with SIRT1 inhibitor increases fat accumulation in HepG2 cells.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"877-885"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140847847","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Omentin roles in physiology and pathophysiology: an up-to-date comprehensive review.","authors":"Aida A Hussein, Noha A Ahmed, Hader I Sakr, Tarek Atia, Osama M Ahmed","doi":"10.1080/13813455.2023.2283685","DOIUrl":"10.1080/13813455.2023.2283685","url":null,"abstract":"<p><p>Omentin (intelectin) was first detected in the visceral omental adipose tissue. It has mainly two isoforms, omentin-1 and -2, with isoform-1 being the main form in human blood. It possesses insulin-sensitizing, anti-inflammatory, anti-atherogenic, cardio-protective, and oxidative stress-decreasing effects. Omentin's cardiovascular protective actions are caused by the improved endothelial cell survival and function, increased endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) bioavailability, enhanced vascular smooth muscle cells (VSMCs) relaxation with reduced proliferation, decreased inflammation, and suppressed oxidative stress. Omentin may also have a potential role in different cancer types and rheumatic diseases. Thus, omentin is an excellent therapeutic target in many diseases, including diabetes mellitus (DM), metabolic syndrome (MetS), cardiovascular diseases (CVDs), inflammatory diseases, and cancer. This review demonstrates the physiological functions of omentin in ameliorating insulin resistance (IR), vascular function, and inflammation and its possible share in managing obesity-linked diseases, such as metabolic disorders, DM, and cardiovascular conditions.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"800-813"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138294552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A review of the last decade: pancreatic cancer and type 2 diabetes.","authors":"Jiaqi Wu, Liang Tang, Feng Zheng, Xun Chen, Lei Li","doi":"10.1080/13813455.2023.2252204","DOIUrl":"10.1080/13813455.2023.2252204","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is a prevalent gastrointestinal tumour known for its high degree of malignancy, resulting in a mere 10% five-year survival rate for most patients. Over the past decade, a growing body of research has shed light on the intricate bidirectional association between PC and Type 2 diabetes (T2DM). The collection of PC- and T2DM-related articles is derived from two comprehensive databases, namely WOS (Web of Science Core Collection) and CNKI (China National Knowledge Infrastructure). This article discusses the last 10 years of research trends in PC and T2DM and explores their potential regulatory relationship as well as related medications.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"660-668"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10486862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dapagliflozin attenuates high glucose-and hypoxia/reoxygenation-induced injury via activating AMPK/mTOR-OPA1-mediated mitochondrial autophagy in H9c2 cardiomyocytes.","authors":"Weiling Tu, Liang Li, Ming Yi, Junyu Chen, Xiaoqing Wang, Yan Sun","doi":"10.1080/13813455.2023.2252200","DOIUrl":"10.1080/13813455.2023.2252200","url":null,"abstract":"<p><p>This study investigated the protective effect of dapagliflozin on H9c2 cardiomyocyte function under high glucose and hypoxia/reoxygenation (HG-H/R) conditions and identified the underlying molecular mechanisms. Dapagliflozin reduced the level of lactate dehydrogenase and reactive oxygen species in cardiomyocytes under HG-H/R conditions and was accompanied by a decrease in caspase-3/9 activity. In addition, Dapagliflozin significantly reduced mitochondrial permeability transition pore opening and increased ATP content, accompanied by upregulation of OPA1 with autophagy-related protein molecules and activation of the AMPK/mTOR signalling pathway in HG-H/R treated cardiomyocytes. OPA1 knockdown or compound C treatment attenuated the protective effects of dapagliflozin on the cardiomyocytes under HG-H/R conditions. Downregulation of OPA1 expression increased mitochondrial intolerance in cardiomyocytes during HG-H/R injury and the AMPK-mTOR-autophagy signalling is a key mechanism for protecting mitochondrial function and reducing cardiomyocyte apoptosis. Collectively, dapagliflozin exerted protective effects on the cardiomyocytes under HG-H/R conditions. Dapagliflozin attenuated myocardial HG-H/R injury by activating AMPK/mTOR-OPA1-mediated mitochondrial autophagy.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"649-659"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10127097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Betaine regulates steroidogenesis, endoplasmic reticulum stress response and Nrf2/HO-1 antioxidant pathways in mouse Leydig cells under hyperglycaemia condition.","authors":"Mohammad Reza Tabandeh, Elahe Davoodi, Vahid Bayati, Dian Dayer","doi":"10.1080/13813455.2023.2272588","DOIUrl":"10.1080/13813455.2023.2272588","url":null,"abstract":"<p><p>We studied the effects of betaine on steroidogenesis, endoplasmic reticulum stress and Nrf2 antioxidant pathways of mice Leydig cells under hyperglycaemia conditions. Leydig cells were grown in low and high glucose concentrations (5 mM and 30 mM) in the presence of 5 mM of betaine for 24 h. Gene expression was determined using a real-time PCR method. The protein levels were determined by Western blot analysis. The testosterone production was evaluated by the ELISA method. Cellular contents of reduced and oxidised glutathione were measured by colorimetric method. Hyperglycaemia caused impaired steroidogenesis and ERS in Leydig cells associated with the down-regulation of 3β-HSD, StAR, P450scc, LH receptor and increased expression of GRP78, CHOP, ATF6 and IRE1. Betaine could improve cell viability, attenuate the ERS, and restore testosterone production in Leydig cells under hyperglycaemia conditions. Betaine can protect Leydig cells against the adverse effects of hyperglycaemia by regulating steroidogenesis, antioxidants, and ERS.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"768-778"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49688562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactate entrance into the brain facilities adipose tissue lipolysis during exercise via circulating calcitonin gene-related peptide.","authors":"Malihe Aveseh, Maryam Koushkie-Jahromi, Javad Nemati, Saeed Esmaeili-Mahani, Najmeh Sadat Hosseini","doi":"10.1080/13813455.2023.2283684","DOIUrl":"10.1080/13813455.2023.2283684","url":null,"abstract":"<p><strong>Objectives: </strong>We assessed the relationships between CGRP, lactate and fat regulation.</p><p><strong>Methods: </strong>We evaluated the effect of intracerebroventricular (i.c.v.) injection of lactate and acute exercise on brain CGRP expression, and its concentration in serum/cerebrospinal fluid (SCF) in rats.</p><p><strong>Results: </strong>Injection of lactate up-regulated CGRP expression in the cortex and CSF and activated p38-mitogen-activated protein kinases (p38-MAPK) pathway. Co-injection of lactate and sb203580, deterred lactate-induced up-regulation of CGRP in the brain and CSF. Exercise increased the CGRP expression in the brain and CSF and up-regulated fat metabolism. Inhibition of lactate entrance into the brain using alpha-cyano-4-hydroxycinnamate (4-CIN) diminished exercise-induced CGRP up-regulation in the brain and CSF. Reducing the circulating blood lactate by pre-treatment of the animals with dichloroacetate (DCA) had no effect on exercise-induced increase in CGRP expression or fat metabolism during exercise.</p><p><strong>Conclusions: </strong>Lactate probably acts as one of a signalling molecule in the brain to regulate fat metabolism during exercise.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"790-799"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138046096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}