Pub Date : 2024-08-05DOI: 10.1080/13813455.2024.2387693
Chunling Zhang, Jie Xiang, Gengxin Wang, Tietao Di, Lu Chen, Wei Zhao, Lianggang Wei, Shiyong Zhou, Xueli Wu, Yun Zhang, Yanhui Wang, Haiyan Liu
Diabetic skin wound is a disturbing and rapidly evolving clinical issue. Here, we investigated how salvianolic acid B (Sal B) affected the diabetic wound healing process. Following Sal B administration, histopathological damage was investigated by H&E and Masson staining, and CD34, apoptosis and mitophagy markers were measured by immunofluorescence, immunohistochemistry, and western blotting. Migration, proliferation, and mitochondrial function of high glucose (HG) -induced HMEC-1 cells were measured. The effects of si-Parkin on endothelial cell migration, apoptosis and mitochondrial autophagy were examined. Sal B alleviated inflammatory cell infiltration and promoted angiogenesis in skin wound tissue. Apoptosis and mitophagy were ameliorated by Sal B in diabetic skin wound tissues and HG-induced HMEC-1 cells. Parkin inhibition impaired the migratorypromoted cell apoptosis and inhibited mitophagy of HMEC-1 cells. This finding demonstrated that Sal B promoted diabetic skin wound repair via Pink1/Parkin-mediated mitophagy, improved our understanding of the diabetic wound healing process.
糖尿病皮肤伤口是一个令人不安且发展迅速的临床问题。在此,我们研究了丹酚酸 B(Sal B)对糖尿病伤口愈合过程的影响。服用丹酚酸 B 后,组织病理学损伤通过 H&E 和 Masson 染色法进行检测,CD34、细胞凋亡和有丝分裂标记物通过免疫荧光、免疫组织化学和 Western 印迹法进行检测。测量了高糖(HG)诱导的 HMEC-1 细胞的迁移、增殖和线粒体功能。研究了 si-Parkin 对内皮细胞迁移、凋亡和线粒体自噬的影响。Sal B减轻了皮肤伤口组织的炎症细胞浸润并促进了血管生成。Sal B可改善糖尿病皮肤伤口组织和HG诱导的HMEC-1细胞的凋亡和线粒体自噬。抑制Parkin可抑制HMEC-1细胞的迁移促进细胞凋亡和有丝分裂。这一发现证明了 Sal B 通过 Pink1/Parkin 介导的有丝分裂促进了糖尿病皮肤伤口的修复,增进了我们对糖尿病伤口愈合过程的了解。
{"title":"Salvianolic acid B improves diabetic skin wound repair through Pink1/Parkin-mediated mitophagy.","authors":"Chunling Zhang, Jie Xiang, Gengxin Wang, Tietao Di, Lu Chen, Wei Zhao, Lianggang Wei, Shiyong Zhou, Xueli Wu, Yun Zhang, Yanhui Wang, Haiyan Liu","doi":"10.1080/13813455.2024.2387693","DOIUrl":"https://doi.org/10.1080/13813455.2024.2387693","url":null,"abstract":"<p><p>Diabetic skin wound is a disturbing and rapidly evolving clinical issue. Here, we investigated how salvianolic acid B (Sal B) affected the diabetic wound healing process. Following Sal B administration, histopathological damage was investigated by H&E and Masson staining, and CD34, apoptosis and mitophagy markers were measured by immunofluorescence, immunohistochemistry, and western blotting. Migration, proliferation, and mitochondrial function of high glucose (HG) -induced HMEC-1 cells were measured. The effects of si-Parkin on endothelial cell migration, apoptosis and mitochondrial autophagy were examined. Sal B alleviated inflammatory cell infiltration and promoted angiogenesis in skin wound tissue. Apoptosis and mitophagy were ameliorated by Sal B in diabetic skin wound tissues and HG-induced HMEC-1 cells. Parkin inhibition impaired the migratorypromoted cell apoptosis and inhibited mitophagy of HMEC-1 cells. This finding demonstrated that Sal B promoted diabetic skin wound repair via Pink1/Parkin-mediated mitophagy, improved our understanding of the diabetic wound healing process.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-12"},"PeriodicalIF":2.5,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888323","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}
Phenolic acids derived from plants have beneficial effects on cardiovascular diseases (CVD). Cinnamic acid (CA) is a crucial phenolic acid that can form numerous hydroxycinnamic derivate found in many food groups. We review current data on the cardiovascular pharmacology of CA with a focus on CVD and their risk factors including hyperlipidaemia, obesity, hyperglycaemia, cardiomyopathy and myocardial ischaemia, vascular dysfunction, oxidative stress and inflammation. Both in vivo and in vitro laboratory studies demonstrate the lipid-lowering, anti-obesity, anti-hyperglycemic, cardio-protective and vasorelaxant activities of CA. The protective impacts of CA against CVD occur by inhibiting inflammatory, oxidative, and apoptotic pathways, regulating the genes and enzymes involved in glucose and lipid metabolisms, and promoting vasodilation. This review showed that the most studied and prominent effects of CA are anti-hyperlipidemic and anti-diabetic properties. In conclusion, intake of plant foods rich in CA may reduce CVD risk especially through regulating blood glucose and lipids levels.
从植物中提取的酚酸对心血管疾病(CVD)有益。肉桂酸(CA)是一种重要的酚酸,可形成多种羟基肉桂酸衍生物,存在于多种食物中。我们回顾了目前有关 CA 的心血管药理学数据,重点是心血管疾病及其风险因素,包括高脂血症、肥胖、高血糖、心肌病和心肌缺血、血管功能障碍、氧化应激和炎症。实验室的体内和体外研究都证明,CA 具有降血脂、抗肥胖、降血糖、保护心脏和舒张血管的作用。CA 对心血管疾病的保护作用是通过抑制炎症、氧化和细胞凋亡途径,调节参与葡萄糖和脂质代谢的基因和酶,以及促进血管舒张来实现的。综述显示,研究最多、最突出的 CA 作用是抗高脂血症和抗糖尿病。总之,摄入富含 CA 的植物性食物可降低心血管疾病风险,特别是通过调节血糖和血脂水平。
{"title":"Cardiovascular protective effects of cinnamic acid as a natural phenolic acid: a review.","authors":"Leila Safaeian, Mansooreh Asghari-Varzaneh, Seyed-Sadegh Alavi, Mahnaz Halvaei-Varnousfaderani, Ismail Laher","doi":"10.1080/13813455.2024.2387694","DOIUrl":"https://doi.org/10.1080/13813455.2024.2387694","url":null,"abstract":"<p><p>Phenolic acids derived from plants have beneficial effects on cardiovascular diseases (CVD). Cinnamic acid (CA) is a crucial phenolic acid that can form numerous hydroxycinnamic derivate found in many food groups. We review current data on the cardiovascular pharmacology of CA with a focus on CVD and their risk factors including hyperlipidaemia, obesity, hyperglycaemia, cardiomyopathy and myocardial ischaemia, vascular dysfunction, oxidative stress and inflammation. Both <i>in vivo</i> and <i>in vitro</i> laboratory studies demonstrate the lipid-lowering, anti-obesity, anti-hyperglycemic, cardio-protective and vasorelaxant activities of CA. The protective impacts of CA against CVD occur by inhibiting inflammatory, oxidative, and apoptotic pathways, regulating the genes and enzymes involved in glucose and lipid metabolisms, and promoting vasodilation. This review showed that the most studied and prominent effects of CA are anti-hyperlipidemic and anti-diabetic properties. In conclusion, intake of plant foods rich in CA may reduce CVD risk especially through regulating blood glucose and lipids levels.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-11"},"PeriodicalIF":2.5,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888320","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}
Pub Date : 2024-08-05DOI: 10.1080/13813455.2024.2387710
Manal Moustafa Mahmoud, Mai Mohammed Hassan, Hany El-Sebaee Elsayed, Amal E Fares, Mona M Saber, Laila Ahmed Rashed, Omaima Mohammed Abdelwahed
Type 2 Diabetes mellitus (T2DM) has the potential to impair cardiac function and cause heart failure. We aimed to study the cardioprotective influence of Galactin-3 (Gal-3) inhibitor; modified citrus pectin (MCP) in isoprenaline induced myocardial infarction (MI) in T2DM rats. Forty rats were allocated into 4 groups; groups I and II served as control. T2DM was provoked in groups III and IV by serving them high fat diet followed by a single low dose of Streptozotocin (STZ), then group IV were administered MCP in drinking water for 6 weeks. Groups III and IV were then subcutaneously injected isoprenaline hydrochloride once daily on the last 2 successive days to induce MI. MCP restored echocardiographic parameters with significant decline in Gal-3 area % in cardiac tissue alongside protection against cardiac remodelling. our data showed that there is a protective potential for Gal-3 inhibitor (MCP) against cardiac injury in isoprenaline induced MI in T2DM.
{"title":"Protective effect of Galectin-3 inhibitor against cardiac remodelling in an isoprenaline-induced myocardial infarction in type 2 diabetes.","authors":"Manal Moustafa Mahmoud, Mai Mohammed Hassan, Hany El-Sebaee Elsayed, Amal E Fares, Mona M Saber, Laila Ahmed Rashed, Omaima Mohammed Abdelwahed","doi":"10.1080/13813455.2024.2387710","DOIUrl":"https://doi.org/10.1080/13813455.2024.2387710","url":null,"abstract":"<p><p>Type 2 Diabetes mellitus (T2DM) has the potential to impair cardiac function and cause heart failure. We aimed to study the cardioprotective influence of Galactin-3 (Gal-3) inhibitor; modified citrus pectin (MCP) in isoprenaline induced myocardial infarction (MI) in T2DM rats. Forty rats were allocated into 4 groups; groups I and II served as control. T2DM was provoked in groups III and IV by serving them high fat diet followed by a single low dose of Streptozotocin (STZ), then group IV were administered MCP in drinking water for 6 weeks. Groups III and IV were then subcutaneously injected isoprenaline hydrochloride once daily on the last 2 successive days to induce MI. MCP restored echocardiographic parameters with significant decline in Gal-3 area % in cardiac tissue alongside protection against cardiac remodelling. our data showed that there is a protective potential for Gal-3 inhibitor (MCP) against cardiac injury in isoprenaline induced MI in T2DM.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-14"},"PeriodicalIF":2.5,"publicationDate":"2024-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141888322","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}
Pub Date : 2024-08-02DOI: 10.1080/13813455.2024.2386279
Emine Kacar, Zeynep Dila Oz, Ihsan Serhatlioglu, Nalan Kaya Tektemur, Mehmet Ridvan Ozdede, Tugce Yalcin, Gulendam Ozbeg, Aslisah Ozgen, Fatih Tan, Seval Ulku Orhan, Ozge Zorlu, Aysun Ucer, Abdullah Yasar, Bayram Yilmaz, Haluk Kelestimur
Objective: To investigate the comprehensive effects of daily chronic asprosin administration on various pubertal and reproductive parameters in female rats. This study aims to elucidate the role of asprosin in regulating the onset of puberty and its influence on hormonal profiles and ovarian histology.
Methods: Asprosin was administered intraperitoneally (i.p.) at a dose of 500 ng/kg daily for eight weeks. Hormonal assays and histological analyses were performed to evaluate the effects of asprosin on the onset of puberty and reproductive function.
Results: Daily chronic administration of asprosin accelerated the onset of the first oestrus. Hormonal assays revealed significant elevations in serum levels of Follicle-Stimulating Hormone (FSH) and Oestradiol (E2), while Inhibin B levels decreased. Histological evaluations demonstrated an increased number of primary and secondary follicles in ovarian tissue, without affecting primordial follicle counts or reproductive organ weights.
Conclusions: Role of adipokines in regulating puberty and reproductive function has increasingly gained recognition. This study aimed to provide the first comprehensive examination of the effects of daily chronic asprosin administration on pubertal and reproductive parameters in female rats. Utilising hormonal assays and histological analyses, asprosin was administered intraperitoneally (i.p.) at a dose of 500 ng/kg, daily, for eight weeks. Our findings revealed that daily chronic administration of asprosin accelerated the onset of the first oestrus. Hormonal assays showed significant elevations in serum levels of Follicle-Stimulating Hormone (FSH) and Oestradiol (E2), while Inhibin B levels decreased. Histological evaluations demonstrated an increased number of primary and secondary follicles in ovarian tissue, without affecting primordial follicle counts or reproductive organ weights. These results provide new insights into asprosin's role in advancing the age of first oestrus and modulating hormonal profiles, thereby offering potential benefits to the female reproductive system.
{"title":"Asprosin-induced alterations in female rat puberty and reproductive hormonal profiles.","authors":"Emine Kacar, Zeynep Dila Oz, Ihsan Serhatlioglu, Nalan Kaya Tektemur, Mehmet Ridvan Ozdede, Tugce Yalcin, Gulendam Ozbeg, Aslisah Ozgen, Fatih Tan, Seval Ulku Orhan, Ozge Zorlu, Aysun Ucer, Abdullah Yasar, Bayram Yilmaz, Haluk Kelestimur","doi":"10.1080/13813455.2024.2386279","DOIUrl":"https://doi.org/10.1080/13813455.2024.2386279","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the comprehensive effects of daily chronic asprosin administration on various pubertal and reproductive parameters in female rats. This study aims to elucidate the role of asprosin in regulating the onset of puberty and its influence on hormonal profiles and ovarian histology.</p><p><strong>Methods: </strong>Asprosin was administered intraperitoneally (i.p.) at a dose of 500 ng/kg daily for eight weeks. Hormonal assays and histological analyses were performed to evaluate the effects of asprosin on the onset of puberty and reproductive function.</p><p><strong>Results: </strong>Daily chronic administration of asprosin accelerated the onset of the first oestrus. Hormonal assays revealed significant elevations in serum levels of Follicle-Stimulating Hormone (FSH) and Oestradiol (E2), while Inhibin B levels decreased. Histological evaluations demonstrated an increased number of primary and secondary follicles in ovarian tissue, without affecting primordial follicle counts or reproductive organ weights.</p><p><strong>Conclusions: </strong>Role of adipokines in regulating puberty and reproductive function has increasingly gained recognition. This study aimed to provide the first comprehensive examination of the effects of daily chronic asprosin administration on pubertal and reproductive parameters in female rats. Utilising hormonal assays and histological analyses, asprosin was administered intraperitoneally (i.p.) at a dose of 500 ng/kg, daily, for eight weeks. Our findings revealed that daily chronic administration of asprosin accelerated the onset of the first oestrus. Hormonal assays showed significant elevations in serum levels of Follicle-Stimulating Hormone (FSH) and Oestradiol (E2), while Inhibin B levels decreased. Histological evaluations demonstrated an increased number of primary and secondary follicles in ovarian tissue, without affecting primordial follicle counts or reproductive organ weights. These results provide new insights into asprosin's role in advancing the age of first oestrus and modulating hormonal profiles, thereby offering potential benefits to the female reproductive system.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-9"},"PeriodicalIF":2.5,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141874052","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}
Pub Date : 2024-08-01Epub Date: 2023-01-03DOI: 10.1080/13813455.2022.2163261
Wenqian Zhang, Xiao-Huan Liu, Jin-Ting Zhou, Cheng Cheng, Jing Xu, Jun Yu, Xiaoming Li
Background: One of the pathological characteristics of obesity is fat accumulation of skeletal muscles (SKM) and the myocardium, involving mechanisms of insulin resistance and abnormal lipid metabolism. Apolipoprotein A-IV (ApoA-IV) is an essential gene in both glucose and lipid metabolisms.
Materials and methods: Using high-fat diet (HFD) induced obese apoA-IV-knockout mice and subsequent introduction of exogenous recombinant-ApoA-IV protein and adeno-associated virus (AAV)-transformed apoA-IV, we examined lipid metabolism indicators of SKM and the myocardium, which include triglyceride (TG) content, RT-PCR for lipogenic indicators and western blotting for AKT phosphorylation. Similarly, we used high-glucose-fed or palmitate (Pal)-induced C2C12 cells co-cultured with ApoA-IV protein to evaluate glucose uptake, the phosphoinositide 3-kinase (PI3K)-AKT pathway, and lipid metabolisms.
Results: In stable obese animal models, we find ApoA-IV-knockout mice show elevated TG content, enhanced expression of lipogenic enzymes and diminished phosphorylated AKT in SKM and the myocardium, but both stable hepatic expression of AAV-apoA-IV and brief ApoA-IV protein administration suppress lipogenesis and promote AKT phosphorylation. In a myoblast cell line C2C12, ApoA-IV protein suppresses Pal-induced lipid accumulation and lipogenesis but enhances AKT activation and glucose uptake, and the effect is abolished by a PI3K inhibitor.
Conclusion: We find that ApoA-IV reduces fat accumulation by suppressing lipogenesis and improves glucose uptake in SKM and the myocardium by regulating the PI3K-AKT pathway.
{"title":"Apolipoprotein A-IV restrains fat accumulation in skeletal and myocardial muscles by inhibiting lipogenesis and activating PI3K-AKT signalling.","authors":"Wenqian Zhang, Xiao-Huan Liu, Jin-Ting Zhou, Cheng Cheng, Jing Xu, Jun Yu, Xiaoming Li","doi":"10.1080/13813455.2022.2163261","DOIUrl":"10.1080/13813455.2022.2163261","url":null,"abstract":"<p><strong>Background: </strong>One of the pathological characteristics of obesity is fat accumulation of skeletal muscles (SKM) and the myocardium, involving mechanisms of insulin resistance and abnormal lipid metabolism. Apolipoprotein A-IV (ApoA-IV) is an essential gene in both glucose and lipid metabolisms.</p><p><strong>Materials and methods: </strong>Using high-fat diet (HFD) induced obese <i>apoA-IV</i>-knockout mice and subsequent introduction of exogenous recombinant-ApoA-IV protein and adeno-associated virus (AAV)-transformed <i>apoA-IV</i>, we examined lipid metabolism indicators of SKM and the myocardium, which include triglyceride (TG) content, RT-PCR for lipogenic indicators and western blotting for AKT phosphorylation. Similarly, we used high-glucose-fed or palmitate (Pal)-induced C2C12 cells co-cultured with ApoA-IV protein to evaluate glucose uptake, the phosphoinositide 3-kinase (PI3K)-AKT pathway, and lipid metabolisms.</p><p><strong>Results: </strong>In stable obese animal models, we find ApoA-IV-knockout mice show elevated TG content, enhanced expression of lipogenic enzymes and diminished phosphorylated AKT in SKM and the myocardium, but both stable hepatic expression of AAV-<i>apoA-IV</i> and brief ApoA-IV protein administration suppress lipogenesis and promote AKT phosphorylation. In a myoblast cell line C2C12, ApoA-IV protein suppresses Pal-induced lipid accumulation and lipogenesis but enhances AKT activation and glucose uptake, and the effect is abolished by a PI3K inhibitor.</p><p><strong>Conclusion: </strong>We find that ApoA-IV reduces fat accumulation by suppressing lipogenesis and improves glucose uptake in SKM and the myocardium by regulating the PI3K-AKT pathway.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"491-501"},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10468663","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}
Type 2 diabetes mellitus (T2DM) is a serious endocrine and metabolic disease that is highly prevalent and causes high mortality and morbidity rates worldwide. This review aims to focus on the potential of probiotics in the management of T2DM and its complications and to summarise the various mechanisms of action of probiotics with respect to T2DM. In this review, experimental studies conducted between 2016 and 2022 were explored. The possible mechanisms of action are based on their ability to modulate the gut microbiota, boost the production of short-chain fatty acids (SCFAs) and glucagon-like peptides, inhibit α-glucosidase, elevate sirtuin 1 (SIRT1) levels while reducing fetuin-A levels, and regulate the level of inflammatory cytokines. This review recommends carrying out further studies, especially human trials, to provide robust evidence-based knowledge on the use of probiotics for the treatment of T2DM.IMPACT STATEMENTT2DM is prevalent worldwide causing high rates of morbidity and mortality.Gut microbiota play a significant role in the pathogenesis of T2DM.Probiotics can be used as possible therapeutic tools for the management of T2DM.The possible mechanisms of action of probiotics include modulation of the gut microbiota, production of SCFAs and glucagon-like peptides, inhibition of α-glucosidase, raising SIRT1, reducing fetuin-A levels, and regulating the level of inflammatory cytokines.
{"title":"The predicted mechanisms and evidence of probiotics on type 2 diabetes mellitus (T2DM).","authors":"Ousman Bajinka, Kodzovi Sylvain Dovi, Lucette Simbilyabo, Ishmail Conteh, Yurong Tan","doi":"10.1080/13813455.2022.2163260","DOIUrl":"10.1080/13813455.2022.2163260","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) is a serious endocrine and metabolic disease that is highly prevalent and causes high mortality and morbidity rates worldwide. This review aims to focus on the potential of probiotics in the management of T2DM and its complications and to summarise the various mechanisms of action of probiotics with respect to T2DM. In this review, experimental studies conducted between 2016 and 2022 were explored. The possible mechanisms of action are based on their ability to modulate the gut microbiota, boost the production of short-chain fatty acids (SCFAs) and glucagon-like peptides, inhibit α-glucosidase, elevate sirtuin 1 (SIRT1) levels while reducing fetuin-A levels, and regulate the level of inflammatory cytokines. This review recommends carrying out further studies, especially human trials, to provide robust evidence-based knowledge on the use of probiotics for the treatment of T2DM.IMPACT STATEMENTT2DM is prevalent worldwide causing high rates of morbidity and mortality.Gut microbiota play a significant role in the pathogenesis of T2DM.Probiotics can be used as possible therapeutic tools for the management of T2DM.The possible mechanisms of action of probiotics include modulation of the gut microbiota, production of SCFAs and glucagon-like peptides, inhibition of α-glucosidase, raising SIRT1, reducing fetuin-A levels, and regulating the level of inflammatory cytokines.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"475-490"},"PeriodicalIF":2.5,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10515823","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}
Context: Polycystic ovary syndrome (PCOS) is an endocrine gynaecological disorder that affects many women of childbearing age.
Objective: To evaluate the efficacy and safety of glucose-like peptide-1 receptor agonists for obese women with PCOS.
Methods: 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.
Results: 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.
Conclusions: 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.
{"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":"https://doi.org/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":"1-7"},"PeriodicalIF":2.5,"publicationDate":"2024-07-31","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}
Pub Date : 2024-07-27DOI: 10.1080/13813455.2024.2376815
Huimin Huang, Yangyong Huang
Background: This study aimed to explore the molecular mechanism of homeodomain-interacting protein kinase 2 (HIPK2) in diabetic foot ulcers (DFU).
Methods: 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.
Results: 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.
Conclusion: Our study revealed that USP7-stabilised HIPK2 contributed to HG-induced HUVECs dysfunctions, thus accelerating DFU process.
{"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":"https://doi.org/10.1080/13813455.2024.2376815","url":null,"abstract":"<p><p><b>Background:</b> This study aimed to explore the molecular mechanism of homeodomain-interacting protein kinase 2 (HIPK2) in diabetic foot ulcers (DFU).</p><p><p><b>Methods:</b> 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><p><b>Results:</b> 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><p><b>Conclusion:</b> 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":"1-8"},"PeriodicalIF":2.5,"publicationDate":"2024-07-27","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}
Pub Date : 2024-07-17DOI: 10.1080/13813455.2024.2377381
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
Objectve: 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.
Materials and methods: Blood pressure, creatinine, urea levels, urinary glucose, urine volume, and protein excretion were reduced in trained SHR-STZ rats.
Results: 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.
Conclusion: 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.
研究目的研究目的:探讨有氧训练对高血压和糖尿病(SHR-STZ)大鼠肾功能、氧化应激、肾内肾素-血管紧张素系统和死亡率的影响:材料和方法:训练后的 SHR-STZ 大鼠的血压、肌酐、尿素水平、尿糖、尿量和蛋白质排泄量均有所降低:结果:有氧训练不仅减轻了氧化应激,还提高了SHR-STZ大鼠肾脏中抗氧化酶的活性。训练提高了肾脏内血管紧张素转换酶(ACE和ACE2)的水平以及肾酶(NEP)的活性,同时降低了肾脏内血管紧张素II(Ang II)的水平。有氧训练明显提高了 STZ-SHR 大鼠的存活率:结论:有氧训练的保护作用与肾脏抗氧化能力的提高、尿蛋白排泄量的减少以及肾内血管紧张素 II 水平的降低和 NEP 活性的提高有关。这些发现可能反映了在高血压和糖尿病的综合病理条件下,大鼠的存活率更高。
{"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":"https://doi.org/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":"1-13"},"PeriodicalIF":2.5,"publicationDate":"2024-07-17","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}
Pub Date : 2024-07-11DOI: 10.1080/13813455.2024.2376812
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
Context: 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.
Objective: Herein, the hepatorenal protective effect of tert-butylhydroquinone (tBHQ) in cisplatin (CDDP)-treated rats was examined.
Methods: 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.
Results: 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.
Significance: Pre-intervention with tBHQ attenuates hepatorenal toxicity of CDDP by dampening oxidative stress, inflammation and apoptosis.
{"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":"https://doi.org/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":"1-11"},"PeriodicalIF":2.5,"publicationDate":"2024-07-11","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}