Archives of Physiology and Biochemistry最新文献

{"title":"Acylated ghrelin protection inhibits apoptosis in the remote myocardium post-myocardial infarction by inhibiting calcineurin and activating ARC.","authors":"Refaat A Eid","doi":"10.1080/13813455.2021.2017463","DOIUrl":"10.1080/13813455.2021.2017463","url":null,"abstract":"<p><p>This study investigated if acylated ghrelin (AG) could inhibit myocardial infarction (MI)-induced apoptosis in the left ventricles (LV) of male rats and tested if this protection involves modulating ARC anti-apoptotic protein. Rats (<i>n</i> = 12/group) were assigned as a sham-operated, a sham + AG (100 µg/kg, 2x/d, S.C.), MI, and MI + AG. With no antioxidant activity or expression of FAS, AG inhibited caspase-3, 8, and 9 and decreased cytosolic/mitochondrial levels of cytochrome-c, Bax, Bad, and Bad-BCL-2 complex in the LVs of the sham-operated and MI-treated rats. Concomitantly, AG preserved the mitochondria structure, decreased mtPTP, and enhanced state-3 respiration in the LVs of both treated groups. These effects were associated with increased mitochondrial levels of ARC and a reduction in the activity of calcineurin. Overall, AG suppresses MI-induced ventricular apoptosis by inhibition of calcineurin, activation of ARC, and preserving mitochondria integrity.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"215-229"},"PeriodicalIF":3.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39771454","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":"Crosstalk between obesity and cancer: a role for adipokines.","authors":"Zoya Tahergorabi, Hamed Lotfi, Maryam Rezaei, Mohammad Aftabi, Mitra Moodi","doi":"10.1080/13813455.2021.1988110","DOIUrl":"10.1080/13813455.2021.1988110","url":null,"abstract":"<p><p>Adipose tissue is a complex organ that is increasingly being recognised as the largest endocrine organ in the body. Adipocytes among multiple cell types of adipose tissue can secrete a variety of adipokines, which are involved in signalling pathways and these can be changed by obesity and cancer. There are proposed mechanisms to link obesity/adiposity to cancer development including adipocytokine dysregulation. Among these adipokines, leptin acts through multiple pathways including the STAT3, MAPK, and PI3K pathways involved in cell growth. Adiponectin has the opposite action from leptin in tumour growth partly because of increased apoptotic responses of p53 and Bax. Visfatin increases cancer cell proliferation through ERK1/2, PI3K/AKT, and p38 which are stimulated by proinflammatory cytokines. Omentin through the PI3K/Akt-Nos pathway is involved in cancer-tumour development. Apelin might be involved through angiogenesis in tumour progressions. PAI-1 via its anti-fibrinolytic activity on cell adhesion and uPA/uPAR activity influence cancer cell growth.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"155-168"},"PeriodicalIF":3.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39538880","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":"Long non-coding RNAs as emerging regulators of miRNAs and epigenetics in diabetes-related chronic kidney disease.","authors":"Vishwadeep Shelke, Ajinath Kale, Himanshu Sankrityayan, Hans-Joachim Anders, Anil Bhanudas Gaikwad","doi":"10.1080/13813455.2021.2023580","DOIUrl":"10.1080/13813455.2021.2023580","url":null,"abstract":"<p><p>Diabetes is one of the major cause of chronic kidney disease (CKD), including \"diabetic nephropathy,\" and is an increasingly prevalent accelerator of the progression of non-diabetic forms of CKD. The long non-coding RNAs (lncRNAs) have come into the limelight in the past few years as one of the emerging weapons against CKD in diabetes. Available data over the past few years demonstrate the interaction of lncRNAs with miRNAs and epigenetic machinery. Interestingly, the evolving data suggest that lncRNAs play a vital role in diabetes-associated CKD by regulation of epigenetic enzymes such as DNA methyltransferase, histone deacetylases, and histone methyltransferases. LncRNAs are also engaged in the regulation of several miRNAs in diabetic nephropathy. Hence this review will elaborate on the association between lncRNAs and their interaction with epigenetic regulators involved in different aspects and thus the progression of CKD in diabetes.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"230-241"},"PeriodicalIF":3.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39788471","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":"Swertiamarin mitigates nephropathy in high-fat diet/streptozotocin-induced diabetic rats by inhibiting the formation of advanced glycation end products.","authors":"Kirti Parwani, Farhin Patel, Pranav Bhagwat, Haritha Dilip, Dhara Patel, Vijay Thiruvenkatam, Palash Mandal","doi":"10.1080/13813455.2021.1987478","DOIUrl":"10.1080/13813455.2021.1987478","url":null,"abstract":"<p><strong>Context: </strong>The molecular mechanism by which Swertiamarin (SM) prevents advanced glycation end products (AGEs) induced diabetic nephropathy (DN) has never been explored.</p><p><strong>Objective: </strong>To evaluate the effect of SM in preventing the progression of DN in high fat diet-streptozotocin-induced diabetic rats.</p><p><strong>Materials and methods: </strong>After 1 week of acclimatisation, the rats were divided randomly into five groups as follows: (1) Control group, which received normal chow diet; (2) High-fat diet (HFD) group which was fed diet comprising of 58.7% fat, 27.5% carbohydrate and 14.4% protein); (3) Aminoguanidine (AG) group which received HFD + 100 mg/k.b.w.AG (intraperitoneal); (4) Metformin (Met) group which received HFD + 70 mg/k.b.w. the oral dose of Met and (5) SM group which was supplemented orally with 50 mg/k.b.w.SM along with HFD. After 12 weeks all HFD fed animals were given a single 35 mg/k.b.w. dose of streptozotocin with continuous HFD feeding for additional 18 weeks. Later, various biochemical assays, urine analyses, histopathological analysis of kidneys, levels of AGEs, expression of various makers, and <i>in-silico</i> analysis were performed.</p><p><strong>Results: </strong>The diabetic group demonstrated oxidative stress, increased levels of AGEs, decreased renal function, fibrosis in the renal tissue, higher expression of the receptor for advanced glycation end products (RAGE), which were ameliorated in the SM treated group. <i>In-silico</i> analysis suggests that SM can prevent the binding of AGEs with RAGE.</p><p><strong>Conclusions: </strong>SM ameliorated DN by inhibiting the oxidative stress induced by AGEs.HighlightsSM reduces the levels of hyperglycaemia-induced advanced glycation end products in serum and renal tissue.SM prevents renal fibrosis by inhibiting the EMT in the kidney tissue.The <i>in-silico</i> analysis proves that SM can inhibit the binding of various AGEs with RAGE, thereby inhibiting the AGE-RAGE axis.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"136-154"},"PeriodicalIF":3.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39527218","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":"Vanillin improves glucose homeostasis and modulates metabolic activities linked to type 2 diabetes in fructose-streptozotocin induced diabetic rats.","authors":"Veronica F Salau, Ochuko L Erukainure, Kolawole O Olofinsan, Nontokozo Z Msomi, Omamuyovwi M Ijomone, Md Shahidul Islam","doi":"10.1080/13813455.2021.1988981","DOIUrl":"10.1080/13813455.2021.1988981","url":null,"abstract":"<p><strong>Objective: </strong>This study investigated the antidiabetic effect of vanillin using <i>in vitro</i>, <i>in silico</i>, and <i>in vivo</i> experimental models.</p><p><strong>Methodology: </strong>Type 2 diabetes (T2D) was induced in male Sprague-Dawley (SD) rats using fructose-streptozotocin (STZ), then orally administered low (150 mg/kg bodyweight) or high (300 mg/kg bodyweight) dose of vanillin for 5 weeks intervention period.</p><p><strong>Results: </strong>Vanillin suppressed the levels of blood glucose, serum cholesterol, triglyceride, low-density lipoprotein cholesterol (LDL-c), alanine transaminase (ALT), aspartate transaminase (AST), creatinine, urea, uric acid, when elevated serum insulin, HDL-cholesterol, and concomitantly improved pancreatic β-cell function, glucose tolerance, and pancreatic morphology. It also elevated both serum and pancreatic tissue GSH level, SOD and catalase activities, and hepatic glycogen level, while depleting malondialdehyde level, α-amylase, lipase, acetylcholinesterase, ATPase, ENTPDase and 5'-nucleotidase, glucose-6-phosphatase, fructose-1,6-bisphosphatase, and glycogen phosphorylase activities.</p><p><strong>Conclusions: </strong>The results indicate the potent antidiabetic effect of vanillin against T2D and its associated complications.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"169-182"},"PeriodicalIF":3.0,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39602907","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":"Wistar rat as an animal model to study high-fat induced kidney damage: a systematic review.","authors":"Renata O Pereira, Luana A Correia, Daniela Farah, Geovana Komoni, Vera Farah, Patricia Fiorino","doi":"10.1080/13813455.2021.2017462","DOIUrl":"10.1080/13813455.2021.2017462","url":null,"abstract":"<p><p>The effects of high-fat-associated kidney damage in humans are not completely elucidated. Animal experiments are essential to understanding the mechanisms underlying human diseases. This systematic review aimed to compile evidence of the role of a high-fat diet during the development of renal lipotoxicity and fibrosis of Wistar rats to understand whether this is a satisfactory model for the study of high fat-induced kidney damage. We conducted systematic searches in PUBMED, EMBASE, Lilacs, and Web of Science databases from inception until May 2021. The risk of bias was assessed using SYRCLE toll. Two reviewers independently screened abstracts and reviewed full-text articles. A total of 11 studies were included. The damage varied depending on the age and sex of the animals, time of protocol, and amount of fat in the diet. In conclusion, the Wistar rat is an adequate animal model to assess the effects of a high-fat diet on the kidneys.HighlightsA high-fat diet may promote kidney damage in Wistar rats.Wistar rat is efficient as an animal model to study high-fat-induced kidney damage.The effect of the diet depends on the fat amount, consumption time, and animal age.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"205-214"},"PeriodicalIF":2.5,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39732437","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":"Isorhamnetin as a potential therapeutic agent for diabetes mellitus through PGK1/AKT activation.","authors":"Abdelrahim Alqudah, Esam Qnais, Mohammed Alqudah, Omar Gammoh, Mohammed Wedyan, Shtaywy S Abdalla","doi":"10.1080/13813455.2024.2323947","DOIUrl":"https://doi.org/10.1080/13813455.2024.2323947","url":null,"abstract":"<p><strong>Context: </strong>Type 2 Diabetes Mellitus (T2D) is a significant health concern worldwide, necessitating novel therapeutic approaches beyond conventional treatments.</p><p><strong>Objective: </strong>To assess isorhamnetin's potential in improving insulin sensitivity and mitigating T2D characteristics through oxidative and glycative stress modulation.</p><p><strong>Materials and methods: </strong>T2D was induced in mice with a high-fat diet and streptozotocin injections. Isorhamnetin was administered at 10 mg/kg for 12 weeks. HepG2 cells were used to examine in vitro effects on stress markers and insulin sensitivity. Molecular effects on the PGK1 and AKT signalling pathway were also analyzed.</p><p><strong>Results: </strong>The administration of isorhamnetin significantly impacted both in vivo and in vitro models. In HepG2 cells, oxidative and glycative stresses were markedly reduced, indicating a direct effect of isorhamnetin on cellular stress pathways, which are implicated in the deterioration of insulin sensitivity. Specifically, treated cells showed a notable decrease in markers of oxidative stress, such as malondialdehyde, and advanced glycation end products, highlighting isorhamnetin's antioxidant and antiglycative properties. In vivo, isorhamnetin-treated mice exhibited substantially lower fasting glucose levels compared to untreated T2D mice, suggesting a strong hypoglycemic effect. Moreover, these mice showed improved insulin responsiveness, evidenced by enhanced glucose tolerance and insulin tolerance tests. The molecular investigation revealed that isorhamnetin activated PGK1, leading to the activation of the AKT signalling pathway, crucial for promoting glucose uptake and reducing insulin resistance. This molecular action underscores the potential mechanism through which isorhamnetin exerts its beneficial effects in T2D management.</p><p><strong>Discussion: </strong>The study underscores isorhamnetin's multifaceted role in T2D management, emphasizing its impact on oxidative and glycative stress reduction and molecular pathways critical for insulin sensitivity.</p><p><strong>Conclusion: </strong>Isorhamnetin presents a promising avenue for T2D treatment, offering a novel approach to enhancing insulin sensitivity and managing glucose levels through the modulation of key molecular pathways. Further research is needed to translate these findings into clinical practice.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-11"},"PeriodicalIF":3.0,"publicationDate":"2024-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038678","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":"Phoenixin-14 protects cardiac damages in a streptozotocin-induced diabetes mice model through SIRT3.","authors":"Bo Yao, Junlin Lv, Le Du, Hui Zhang, Zhao Xu","doi":"10.1080/13813455.2021.1981946","DOIUrl":"10.1080/13813455.2021.1981946","url":null,"abstract":"<p><strong>Background: </strong>Type I diabetes is a metabolic syndrome that severely impacts the normal lives of patients through its multiple complications, such as diabetic cardiomyopathy (DCM). Phoenixin-14 is a peptide found to be widely expressed in eukaryons with multiple protective properties, including anti-oxidative stress and anti-inflammatory effects. The present study aims to explore the potential therapeutic impacts of Phoenixin-14 on DCM.</p><p><strong>Methods: </strong>Type I diabetes was induced by treatment with a single dose of STZ (40 mg/kg body weight) intraperitoneally for 5 consecutive days. Mice were divided into four groups: the Control, Phoenixin-14, T1DM, and Phoenixin-14 +T1DM groups. The levels of myocardial injury markers were measured. Cardiac hypertrophy was assessed using wheat germ agglutinin (WGA) staining.</p><p><strong>Results: </strong>Phoenixin-14 was significantly downregulated in the cardiac tissue of diabetic mice. The myocardial injury and deteriorated cardiac function in diabetic mice induced by STZ were significantly ameliorated by Phoenixin-14, accompanied by the alleviation of cardiac hypertrophy. In addition, the severe oxidative stress and inflammation in diabetic mice were dramatically mitigated by Phoenixin-14. Lastly, the downregulated SIRT3 and upregulated p-FOXO3 in diabetic mice were pronouncedly reversed by Phoenixin-14. It is worth mentioning that compared to the Control, no significant changes to any of the investigated parameters in the present study were found in the Phoenixin-14-treated normal mice, suggesting that treatment with it has no side effects.</p><p><strong>Conclusion: </strong>Our data revealed that Phoenixin-14 protected against cardiac damages in STZ-induced diabetes mice models.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"110-118"},"PeriodicalIF":3.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39495862","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":"Nobiletin ameliorates streptozotocin-cadmium-induced diabetic nephropathy <i>via</i> NF-κB signalling pathway in rats.","authors":"Mingzhu Xu, Ruifang Wang, Hui Fan, Ziyuan Ni","doi":"10.1080/13813455.2021.1959617","DOIUrl":"10.1080/13813455.2021.1959617","url":null,"abstract":"<p><p>This study sought to examine the anti-diabetic effect of nobiletin on streptozotocin (STZ)/cadmium (Cd)-induced diabetic nephrotoxic (DN) rats. The DN was induced using STZ (40 mg/kg b.w) intraperitoneally and Cd through drinking water for 12 weeks. The DN rats were treated with nobiletin of different concentrations (10, 20, and 40 mg/kg/BW). The STZ/Cd-induced DN leads to a significantly increased of the glucose levels, glycosylated haemoglobin, hepatic and kidney function markers, lipid peroxidation levels, and reduction of insulin levels, total haemoglobin, body weight, and antioxidant status markers. Our finding that nobiletin pathological impairment and diminished infiltration of neutrophil in kidney tubules and all biochemical enzymes were near normal levels in DN. More essentially, nobiletin strongly impedes the protein expression of renal nuclear NF-κB p65. Bax protein expression was significantly downregulated and elevated protein expression Bcl-2 was recorded in DN rats. These results show that nobiletin possesses antioxidant as well as anti-diabetic activities and thereby reduces chronic kidney diseases in rats.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"29-37"},"PeriodicalIF":3.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39273772","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":"SIRT1: a promising therapeutic target in type 2 diabetes mellitus.","authors":"Ainaz Mihanfar, Maryam Akbarzadeh, Saber Ghazizadeh Darband, Shirin Sadighparvar, Maryam Majidinia","doi":"10.1080/13813455.2021.1956976","DOIUrl":"10.1080/13813455.2021.1956976","url":null,"abstract":"<p><p>A significant increase in the worldwide incidence and prevalence of type 2 diabetic mellitus (T2DM) has elevated the need for studies on novel and effective therapeutic strategies. Sirtuin 1 (SIRT1) is an NAD + dependent protein deacetylase with a critical function in the regulation of glucose/lipid metabolism, insulin resistance, inflammation, oxidative stress, and mitochondrial function. SIRT1 is also involved in the regulation of insulin secretion from pancreatic β-cells and protecting these cells from inflammation and oxidative stress-mediated tissue damages. In this regard, major SIRT1 activators have been demonstrated to exert a beneficial impact in reversing T2DM-related complications including cardiomyopathy, nephropathy, retinopathy, and neuropathy, hence treating T2DM. Therefore, an accumulating number of recent studies have investigated the efficacy of targeting SIRT1 as a therapeutic strategy in T2DM. In this review we aimed to discuss the current understanding of the physiological and biological roles of SIRT1, then its implication in the pathogenesis of T2DM, and the therapeutic potential of SIRT1 in combating T2DM.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"13-28"},"PeriodicalIF":3.0,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39303583","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}