Archives of Physiology and Biochemistry最新文献

{"title":"Bisphenol A induces non-alcoholic fatty liver disease by promoting the O-GlcNAcylation of NLRP3.","authors":"Yonghong Zhang, Shujuan Han, Tian Li, Li Zhu, Feng Wei","doi":"10.1080/13813455.2023.2288533","DOIUrl":"10.1080/13813455.2023.2288533","url":null,"abstract":"<p><p>Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease. The mechanism by which bisphenol A (BPA) promots NAFLD remains unclear. Palmitic acid (PA) and lipopolysaccharide (LPS) were used to simulate NAFLD in HepG2 cells <i>in vitro</i>. Total cholesterol (TC), triglyceride (TG) content, and lipid accumulation were measured to evaluate lipid metabolism. The caspase-1-stained cells and NLRP3 inflammasome-associated proteins were evaluated for pyroptosis. Western blot analysis was used to detect protein levels and co-immunoprecipitation (Co-IP) was used to detect the association between the proteins. Cycloheximide (CHX) treatment combined with western blot was performed to access protein stability. This data have shown that BPA induces lipid metabolism dysfunction and pyroptosis by upregulating O-GlcNAc transferase (OGT) level. NLRP3 directly interacts with OGT, and elevated OGT enhanced the stability of NLRP3 protein. BPA promoted OGT-mediated O-GlcNAcylation to stabilised NLRP3, thus accelerating NAFLD progress <i>in vitro</i>. Our study reveals that BPA, as an environmental factor, may be involved in the promotion of NAFLD, and that targeting NLRP3 and OGT may inhibit BPA's induction of NAFLD.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"814-822"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138457563","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":"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":"866-876"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","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":"Protective effect of <i>tert</i>-butylhydroquinone against cisplatin-induced hepatorenal injury via modulating oxidative stress, inflammation, and apoptosis.","authors":"Godwin Adakole Ujah, Emmanuel Oleba Ofutet, Catherine Ironya-Ogar Ukam, Precious Evangeline Omiunu, Emaediong Ufot Ackley, Iboro Godwin Japhet, Jane Charles Ntauko, Queen Comfort Clement, Racheal Atu, Victor Udo Nna","doi":"10.1080/13813455.2024.2376812","DOIUrl":"10.1080/13813455.2024.2376812","url":null,"abstract":"<p><strong>Context: </strong>Cisplastin (CDDP) is a chemotherapeutic drug frequently used to manage a variety of cancers. However, its use is associated with hepatorenal toxicity resulting from elevated reactive oxygen species production.</p><p><strong>Objective: </strong>Herein, the hepatorenal protective effect of <i>tert</i>-butylhydroquinone (tBHQ) in cisplatin (CDDP)-treated rats was examined.</p><p><strong>Methods: </strong>Wistar male rats randomly divided into four groups: normal control, tBHQ, CDDP and tBHQ + CDDP received 50 mg/kg b.w./day of tBHQ orally for 14 days while 7 mg/kg b.w of CDDP was administered intraperitoneally on Day 8.</p><p><strong>Results: </strong>CDDP increased serum biomarkers of hepatic (AST, ALP, ALT, GGT) and renal (creatinine, urea, uric acid, kidney injury molecule 1) function. The levels of nuclear factor erythroid-2-related factor 2 protein and the activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase activities were decreased in liver and kidney. Also, CDDP increased hepatic and renal levels of NF-κB, TNFα, Bax and caspase-3 proteins and decreased hepatorenal levels of Bcl-2 protein in the liver and kidney. Pre-treatment with tBHQ prevented these negative effects.</p><p><strong>Significance: </strong>Pre-intervention with tBHQ attenuates hepatorenal toxicity of CDDP by dampening oxidative stress, inflammation and apoptosis.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"951-961"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589455","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":"USP7-stabilised HIPK2 promotes high glucose-induced endothelial cell dysfunctions to accelerate diabetic foot ulcers.","authors":"Huimin Huang, Yangyong Huang","doi":"10.1080/13813455.2024.2376815","DOIUrl":"10.1080/13813455.2024.2376815","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to explore the molecular mechanism of homeodomain-interacting protein kinase 2 (HIPK2) in diabetic foot ulcers (DFU).</p><p><strong>Methods: </strong>High glucose (HG)-induced human umbilical vein endothelial cells (HUVECs) were used to construct DFU cell models. Cell functions were determined using CCK8 assay, EdU assay, flow cytometry, transwell assay, wound healing assay and tube formation assay. Quantitative real-time PCR and western blot were applied to measure the gene expression.</p><p><strong>Results: </strong>HG treatment suppressed HUVECs proliferation, invasion, migration, and angiogenesis, while enhanced apoptosis. HIPK2 was overexpressed in DFU patients, and its knockdown alleviated HG-induced HUVECs dysfunctions. USP7 stabilised HIPK2 protein by reducing its ubiquitination. USP7 overexpression promoted HG-induced HUVECs dysfunctions, and HIPK2 upregulation also reversed the regulation of USP7 knockdown on HG-induced HUVECs dysfunctions. USP7/HIPK2 axis inhibited the activity of PI3K/AKT pathway.</p><p><strong>Conclusion: </strong>Our study revealed that USP7-stabilised HIPK2 contributed to HG-induced HUVECs dysfunctions, thus accelerating DFU process.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"984-991"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141787151","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":"Efficacy and safety of glucagon-like peptide-1 receptor agonists in the treatment of polycystic ovary syndrome-A systematic review and meta-analysis.","authors":"Xin Tong, Xiaoxuan Song, Yingshi Zhang, Qingchun Zhao","doi":"10.1080/13813455.2024.2380422","DOIUrl":"10.1080/13813455.2024.2380422","url":null,"abstract":"<p><strong>Context: </strong>Polycystic ovary syndrome (PCOS) is an endocrine gynaecological disorder that affects many women of childbearing age.</p><p><strong>Objective: </strong>To evaluate the efficacy and safety of glucose-like peptide-1 receptor agonists for obese women with PCOS.</p><p><strong>Methods: </strong>We searched the PubMed, Embase, WOS, and Cochrane Libarary databases up to June 2023. Studies were eligible if they were randomised controlled trials (RCTs) comparing GLP-1RAs against any other treatments for patients with PCOS.</p><p><strong>Results: </strong>Overall, a total of 8 RCTs were included in this review, 7 of the RCTs compared GLP-1RAs with metformin, and 1 RCT compared GLP-1Ras with dapagliflozin. Compared with control group, GLP-1RAs were more effective at improving insulin sensitivity, reducing BMI, and resulting in a smaller waist circumference.</p><p><strong>Conclusions: </strong>GLP-1RAs may be a good option for obese women with PCOS, especially those with insulin resistance. However, high-quality studies are also needed in the future to assess the efficacy of GLP-1RAs in women with PCOS.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1005-1011"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141858917","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":"Exploring plant-based alpha-glucosidase inhibitors: promising contenders for combatting type-2 diabetes.","authors":"Sonali Kumari, Ravi Saini, Aditi Bhatnagar, Abha Mishra","doi":"10.1080/13813455.2023.2262167","DOIUrl":"10.1080/13813455.2023.2262167","url":null,"abstract":"<p><strong>Objective: </strong>This systematic review aimed to provide comprehensive details on the α-G inhibitory potential of various bioactive compounds derived from natural sources.</p><p><strong>Methods: </strong>A comprehensive literature search was conducted using various databases and search engines, including Science Direct, Google Scholar, SciFinder, Web of Science, and PubMed until May, 2023.</p><p><strong>Results and conclusions: </strong>The enzyme alpha-glucosidase (α-G) is found in the brush border epithelium of the small intestine and consists of duplicated glycoside hydrolase (GH31) domain. It involves the conversion of disaccharides and oligosaccharides into monosaccharides by acting on alpha (1 → 4) and (1 → 6) linked glucose residue. Once absorbed, glucose enters the bloodstream and elevates postprandial glucose, which is associated with the development of type 2 Diabetes (T2D). Epidemic obesity, cardiovascular disease, and nephropathy are linked to T2D. Traditional medicinal plants with α-G inhibitory potential are commonly used to treat T2D due to the adverse effects of currently used α-G inhibitors miglitol, acarbose, and voglibose. Various bioactive compounds derived from natural sources, including lupenone, Wilforlide A, Baicalein, Betulinic acid, Ursolic acid, Oleanolic acid, Katononic acid, Carnosol, Hypericin, Astilbin, lupeol, betulonic acid, Fagomine, Lactucaxanthin, Erythritol, GP90-1B, Procyanidins, Galangin, and vomifoliol retain α-G inhibitory potential for regulating hyperglycaemia.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"694-709"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41177977","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":"Carvacrol is potential molecule for diabetes treatment.","authors":"Mustafa Hoca, Eda Becer, Hafize Seda Vatansever","doi":"10.1080/13813455.2023.2288537","DOIUrl":"10.1080/13813455.2023.2288537","url":null,"abstract":"<p><p>Diabetes is an important chronic disease that can lead to various negative consequences and complications. In recent years, several new alternative treatments have been developed to improve diabetes. Carvacrol found in essential oils of numerous plant species and has crucial potential effects on diabetes. The anti-diabetic effects of carvacrol have also been comprehensively studied in diabetic animal and cell models. In addition, carvacrol could improve diabetes through affecting diabetes-related enzymes, insulin resistance, insulin sensitivity, glucose uptake, anti-oxidant, and anti-inflammatory mechanisms. The use of carvacrol alone or in combination with anti-diabetic therapies could show a significant potential effect in the treatment of diabetes. This review contributes an overview of the effect of carvacrol in diabetes and anti-diabetic mechanisms.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"823-830"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138450732","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":"Celastrol attenuates HFD-induced obesity and improves metabolic function independent of adiponectin signaling.","authors":"Ling Ye, Yan Gao, Xuecheng Li, Xiaoshuang Liang, Yi Yang, Rufeng Zhang","doi":"10.1080/13813455.2023.2250929","DOIUrl":"10.1080/13813455.2023.2250929","url":null,"abstract":"<p><strong>Backgound: </strong>Celastrol, a leptin sensitiser, has been shown to inhibit food intake and reduce body weight in diet-induced obese mice, making it a potential treatment for obesity and metabolic diseases. Adiponectin signalling has been reported to play an important role in the treatment of obesity, inflammation, and non-alcoholic fatty liver disease.</p><p><strong>Materials and methods: </strong>Wild-type (WT) and AdipoR1 knockout (AdipoR1^-/-) mice were placed on a chow diet or a high-fat diet (HFD) and several metabolic parameters were measured. Celastrol was then administered to the HFD-induced mice and the response of WT and AdipoR1^-/- mice to celastrol in terms of body weight, blood glucose, and food intake was also recorded.</p><p><strong>Results: </strong>AdipoR1 knockout caused elevated blood glucose and lipids, impaired glucose tolerance and insulin resistance in mice, as well as increased susceptibility to HFD-induced obesity. After 14 days of treatment, WT and AdipoR1^-/- mice showed significant reductions in body weight and blood glucose and improvements in glucose tolerance.</p><p><strong>Conclusion: </strong>The present study demonstrated that AdipoR1 plays a critical role in metabolic regulation and that the improvement of weight and metabolic function by celastrol is independent of the AdipoR1-mediated signalling pathway.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"642-648"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10103207","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":"METTL14 plays an oncogenic role in NSCLC by modulating ferroptosis and the m6A modification of GPX4.","authors":"Yang Lou, Kan Huang, Bo Xu, Xianguo Chen","doi":"10.1080/13813455.2024.2376813","DOIUrl":"10.1080/13813455.2024.2376813","url":null,"abstract":"<p><strong>Context: </strong>N6-methyladenosine (m6A) of RNA is involved in the progression of non-small cell lung cancer (NSCLC).</p><p><strong>Objective: </strong>This study investigated the role of METTL14 in NSCLC and the mechanism.</p><p><strong>Materials and methods: </strong>Expression levels were assessed by quantitative real-time PCR and ELISA assays. Cells viability was assessed by cell counting kit-8. M6A methylation was analysed by methylated RNA immunoprecipitation (MeRIP), RIP, luciferase assay, and mRNA stability assay.</p><p><strong>Results: </strong>The results showed that METTL14 was highly expressed in NSCLC tissues and cell lines. Knockdown of METTL14 inhibited the cell viability while induced ferroptosis of NSCLC cells. Mechanistically, METTL14 interacts with GPX4, mediates m6A modification of GPX4, enhances its mRNA stability, and upregulates its expression. In addition, IGF2BP1 recognises the m6A-methylated GPX4 and mediates the elevated mRNA stability. Moreover, GPX4 reversed the effects of METTL14 depletion.</p><p><strong>Discussion and conclusion: </strong>The METTL14/GPX4 axis promotes NSCLC progression by inhibiting cell ferroptosis through the recognition of m6A modification mediated by IGF2BP1.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"962-973"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141589454","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":"Tomatidine ameliorates high-fat-diet/streptozocin (HFD/STZ)-induced type 2 diabetes mellitus in mice.","authors":"Li Cai, Baojian Hou, Juping Hu","doi":"10.1080/13813455.2023.2298404","DOIUrl":"10.1080/13813455.2023.2298404","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of tomatidine (Td) on the progression of type 2 diabetes mellitus (T2DM) in mice and uncover the mechanism.</p><p><strong>Methods: </strong>T2DM mice model was induced by high-fat diet (HFD) and intrabitoneal injection of streptozotocin (STZ). The mice were grouped as follows: 1, control; 2, T2D; 3, T2D + tomatidine (5 mg/kg); 4, T2D + tomatidine (10 mg/kg); 5, T2D + tomatidine (20 mg/kg). Fasting blood glucose was detected by glucose metre and fasting insulin was detected by the kit to determine the effect of Td on T2DM mice. ELISA, qPCR, and Immunoblot assays were performed to detect the effects of Td on the hepatic glucose homeostasis and inflammation of mice. Immunoblot assays further confirmed the mechanism.</p><p><strong>Results: </strong>Td improved blood glucose and insulin resistance in T2DM mice. In addition, Td improved liver function and lipid metabolism disorder in T2DM mice. Td also affected the liver glucose homeostasis related genes in T2DM mice. Td alleviated serum inflammation in T2DM mice. We further found that Td activated AMPK pathway, therefore ameliorating T2DM.</p><p><strong>Conclusion: </strong>Td ameliorated HFD/STZ-induced T2DM in mice, suggesting that it could serve as a drug of T2DM.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"848-853"},"PeriodicalIF":2.5,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139377147","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}