Journal of physiological investigation最新文献

{"title":"Combination Effect of Caffeine Intake and Thermotherapy on the Blood Levels of Human Irisin and Fibroblast Growth Factor 21 in Healthy Males.","authors":"Hye-Jin Lee, Tae-Hwan Park, Bah-Da Yun, In-Ho Lee, Mid-Eum Moon, Sang-Hyeon Kim, Yi-Rang Lim, Mun-Jeong Kim, Da-Jeong Bae, Jin Kim, Young-Hyun Jung, Jeong-Beom Lee","doi":"10.4103/ejpi.EJPI-D-25-00003","DOIUrl":"https://doi.org/10.4103/ejpi.EJPI-D-25-00003","url":null,"abstract":"<p><strong>Abstract: </strong>Caffeine is a widely consumed psychoactive substance known to influence physiological processes such as heat generation and autonomic nervous system activity. Fibroblast growth factor 21 (FGF-21) and irisin are the biomarkers associated with thermogenesis and metabolic regulation. The study aimed to determine whether thermotherapy along with caffeine intake could increase the blood levels of FGF-21 and irisin. A total of 87 healthy male subjects were randomly divided into a control group and a caffeine intake group. For heat loading, an experiment was performed in which each subject was given a 30-min half-body bath in hot water (42°C ± 0.5°C), and their tympanic temperature (Tty), mean skin temperature (mTs), and serum FGF-21 and irisin levels were measured. Compared to the control group, the caffeine intake group showed significantly increased Tty, mTs, serum FGF-21, and irisin after thermotherapy. Especially, administration of caffeine led to a significantly amplified response in circulating FGF-21 and irisin levels, showing an additional 22.93% and 28.70% increase, respectively, compared to the control group (P < 0.001). The results suggest that as a new form of synergy, the combination of caffeine intake and thermotherapy could potentially be applied to broader clinical and physiological settings.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144602667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CircERBB3 Targets miR-194-5p/PRMT3 to Promote Hepatocellular Carcinoma Progression.","authors":"Shihao Jiang, Zhihao Bai, Jiaxin Li, Ning Zhou","doi":"10.4103/ejpi.EJPI-D-24-00110","DOIUrl":"https://doi.org/10.4103/ejpi.EJPI-D-24-00110","url":null,"abstract":"<p><strong>Abstract: </strong>The role of circular RNAs in the progression of hepatocellular carcinoma (HCC) is still unclear. This study explored the oncogenic properties of circERBB3 in HCC and the underlying molecular mechanisms. After transfection, cell behaviors including proliferation, invasion, migration, and apoptosis were measured by performing Cell Counting Kit-8, transwell, scratch, and flow cytometry assays, respectively. Luciferase reporter genes were employed to analyze the interaction of miR-194-5p with circERBB3 or PRMT3. Quantitative polymerase chain reaction was used to detect circERBB3, miR-194-5p, and PRMT3 mRNA and western blotting was used for PRMT3 protein detection. CircERBB3 and PRMT3 were upregulated in HCC cell lines, while miR-194-5p was expressed at low levels. CircERBB3 knockdown, PRMT3 knockdown, or miR-194-5p overexpression suppressed proliferation, invasion, and migration and accelerated apoptosis in HCC cells. CircERBB3 targeted miR-194-5p and negatively regulated its expression. miR-194-5p targeted PRMT3 and inhibited its expression. miR-194-5p inhibition or PRMT3 overexpression stimulated the malignant behaviors of HCC cells underexpressing circERBB3. In conclusion, circERBB3 targeted miR-194-5p to promote PRMT3 expression, thereby promoting HCC cell malignancy.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Itaconate Attenuates Homocysteine-induced Nod-like Receptor Family Protein 3 Inflammasome-mediated Pyroptosis in Hippocampal Neurons: Involvement of Inhibiting Succinate Dehydrogenase Complex Subunit A Level.","authors":"Min Huang, Pan-Pan Zhang, Yi-Yun Tang, Min Li, Jia-Mei Jiang, Xiao-Qing Tang","doi":"10.4103/ejpi.EJPI-D-25-00018","DOIUrl":"https://doi.org/10.4103/ejpi.EJPI-D-25-00018","url":null,"abstract":"<p><strong>Abstract: </strong>Elevated homocysteine (Hcy) levels are associated with various neurodegenerative diseases. Elucidating the pathogenesis of Hcy-associated neurotoxicity and exploring novel approaches for preventing and treating Hcy-induced neurotoxicity are of paramount significance. This study will be based on nod-like receptor family protein 3 (NLRP3)-mediated pyroptosis and succinate dehydrogenase (SDH) to study the mechanisms underlying the neurotoxicity of Hcy in HT-22 cells, a mouse hippocampal neuronal cell line, and the protective role and mechanisms of itaconate against Hcy-associated neurotoxicity. Cell viability was assessed by CCK-8 assay. The contents of interleukin-1 beta (IL-1β) and IL-18 in the culture supernatant were detected by enzyme-linked immunosorbent assay. The expressions of pyroptosis-related proteins and succinate dehydrogenase complex subunit A (SDHA) were measured by Western blot analysis. The colocalization of gasdermin D (GSDMD) and the cell membrane was observed by Immunofluorescence. Our findings indicate that Hcy treatment significantly decreased HT22 cell viability and increased the inflammatory response. Furthermore, Hcy treatment enhanced GSDMD-N expression level, promoted the membrane localization of GSDMD, and increased the expression levels of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), and cleaved-caspase-1 in HT22 cells. Notably, itaconate reversed the effects of Hcy on neurotoxicity, as evidenced by increased cell viability and decreased NLRP3 inflammasome-mediated pyroptosis in HT22 cells. Furthermore, itaconate reduced the expression level of SDHA in Hcy-exposed HT22 cells. These findings highlight that NLRP3 inflammasome-mediated pyroptosis and the activation of SDHA play crucial roles in Hcy-induced neuronal injury and that itaconate protects against Hcy-induced NLRP3 inflammasome-mediated pyroptosis via suppressing SDHA expression.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144568296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Hyperglycemia on Streptococcus pneumoniae Virulence: Insights into Capsular Dynamics and Clinical Implications.","authors":"Pin Wang","doi":"10.4103/ejpi.EJPI-D-24-00112","DOIUrl":"https://doi.org/10.4103/ejpi.EJPI-D-24-00112","url":null,"abstract":"<p><strong>Abstract: </strong>Hyperglycemia, a diabetic condition, profoundly affects the pathogenicity of Streptococcus pneumoniae ( S . pneumoniae ), a leading etiologic pathogen of pneumonia. This review addresses a systematic understanding of how hyperglycemia affects the pathogenicity of S . pneumoniae , especially by immune dysfunction, cytokine dysregulation, and oxidative stress. Although the length of the capsular polysaccharide (CPS) chain plays a role in immune evasion and survival of bacteria, hyperglycemia also affects host immune responses, leading to increased severity of infection in diabetic patients. CPS length polymorphism, whose wzy gene regulation in the majority of instances is under strict control, avoids immunity by phagocytosis and complement inhibition mechanisms. Metabolic dysregulation secondary to hyperglycemia caused by diabetes with activation of the stress pathways and modifications of the availability of nucleotide sugars potentially results in aberrant CPS polymerization with subsequent augmentation of capsule elongation lengths. These changes facilitate the survival of the bacterium, increase immune dysregulation, and aggravate disease severity in diabetes. Determination of the interaction among hyperglycemia, immune dysfunction, and pneumococcal virulence factors positions the demand for focused therapy to reduce infection risks. This review facilitates awareness of bacterial pathogenesis and public health policy to improve clinical outcomes in high-risk diabetic patients with complicated pneumococcal infection.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144218028","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effect of Thymic Stromal Lymphopoietin on Reflux Esophagitis.","authors":"Ruidong Chen, Longfei Zhao, Yunyun Hu, Hong Li","doi":"10.4103/ejpi.EJPI-D-23-00020","DOIUrl":"https://doi.org/10.4103/ejpi.EJPI-D-23-00020","url":null,"abstract":"<p><strong>Abstract: </strong>Reflux esophagitis (RE) is characterized by the infiltration of inflammatory cells into the damaged squamous epithelium. Thymic stromal lymphopoietin (TSLP) has been implicated in promoting T helper type 2 (Th2) inflammation. This study investigates the protective role of TSLP downregulation in RE. A rat model of RE underwent surgical treatment, while cell model was exposed to an acid and bile mixture. Protein expression levels of TSLP, signal transducer and activator of transcription 3 (STAT3), and Janus tyrosine kinase 2 (JAK2) were assessed using western blot analysis. Interleukin levels (IL-4, IL-5, and IL-13) were quantified via enzyme-linked immunosorbent assay and quantitative polymerase chain reaction (qPCR). Esophageal epithelial barrier function was evaluated through transepithelial electrical resistance (TEER). TSLP levels in esophageal tissue were detected by immunohistochemistry. Elevated protein expression of pro-inflammatory factors TSLP, IL-4, IL-5, and IL-13 was observed in RE. Tezspire treatment reduced inflammatory levels and pathological lesions in esophageal tissue, reversed cell damage, decreased inflammatory cytokines, and enhanced epithelial barrier function. TSLP modulated RE development through JAK/STAT pathway activation. Downregulation of TSLP demonstrated anti-inflammatory effects and mitigated esophageal epithelial injury caused by gastric acid reflux. These findings suggest that TSLP may serve as a novel target for RE treatment.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144218029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Air Quality on the Mucosal Immune Molecules in Outdoor Male Athletes.","authors":"Ming-Ru Chiang, Tung-Lin Lu, Chi-Cheng Lu, Yi-Ying Chen, Shih-Hua Fang","doi":"10.4103/ejpi.EJPI-D-25-00010","DOIUrl":"https://doi.org/10.4103/ejpi.EJPI-D-25-00010","url":null,"abstract":"<p><strong>Abstract: </strong>Elevated concentrations of particulate matter 2.5 (PM2.5) can harm the human respiratory system. Athletes training outdoors in polluted environments may face an increased risk of exposure. Few studies have reported on the effects of air quality on the mucosal immunity of athletes. In this study, we recruited 32 male athletes and employed a randomized crossover design. Each participant provided 2 ml of saliva sample before and after their regular 2-h exercise sessions on days with and without air pollution. The immune molecules in saliva, including immunoglobulin A, lysozyme, α-amylase, and nitric oxide (NO), were measured. The results indicated that exercise on PM2.5-polluted days resulted in significantly higher post-exercise salivary NO levels compared to those on nonpolluted days and led to an increase in α-amylase activity compared to the pre-exercise condition. For the 16 atopic participants, the post-exercise salivary NO levels on PM2.5-polluted days were significantly elevated than nonpolluted days. Although athletes without a history of allergic conditions exhibited similar changes, the magnitude of these responses was less pronounced. In conclusion, PM2.5 pollution induces physiological stress and inflammatory responses in athletes, particularly those with allergies. More research is needed to determine the chronic effects of air quality on the mucosal immunity of outdoor athletes.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144176499","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential Transcription Factor Activator Protein-2 Delta Genotypes Affect the Levels of Interleukin-1 Beta, Interleukin 8, and Vascular Endothelial Growth Factor-C in the Retinal Pigment Epithelial Cells after Long-term Light Exposure.","authors":"Chih-Hui Chin, Chih-Cheng Chien, Chi-Jung Huang, Chia-Ying Ke, Yih-Jing Lee","doi":"10.4103/ejpi.EJPI-D-24-00107","DOIUrl":"https://doi.org/10.4103/ejpi.EJPI-D-24-00107","url":null,"abstract":"<p><strong>Abstract: </strong>Retinal degeneration accompanied by abnormal neovascularization from the choroid in the macular area is a critical disease to cure. Retinal cell apoptosis or inflammation in the macula can lead to neovascularization in that area. Some environmental factors such as long-term light exposure, particularly the blue end of the light spectrum, can damage the retina, causing such a disease. Improved understanding of genetic molecules has indicated that certain genes may be potential biomarkers of neovascular macular degeneration. This study aimed to investigate the expression of transcription factor activator protein-2 δ (TFAP-2D) in the retina and explore its role in the pathogenesis of retinal degeneration. For this, a long-term light exposure animal model was used to evaluate TFAP-2D expression in the retina. In addition, two vectors overexpressing different genotypes of TFAP-2D were transfected into retinal pigment epithelial (RPE) cells, and the expression of angiogenesis molecules was investigated. It was found that TFAP-2D expression was observed in the RPE area of the retina in long-term light-exposed rats; however, no TFAP-2D expression was detected in the retina of control (normal) rats. Interleukins (ILs) 1B, IL8, vascular endothelial growth factor (VEGF)-C, and one VEGF receptor (kinase insert domain receptor) were significantly upregulated in RPE cells with TFAP-2D with a C allele at rs78648104 (TFAP-2D-C) overexpression. In conclusion, experiments with different TFAP-2D genotypes revealed that long-term light exposure upregulated TFAP-2D expression in the RPE cells of the retina. In addition, overexpression of TFAP-2D-C induced the release of IL1B, IL8, and VEGF-C, which may lead to neovascularization in the choroid and retina.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144113271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extracts of Chuanxiong and Baizhi Attenuate Neuroinflammation in Chronic Migraine Rats by Inhibiting TLR4/MyD88/Nuclear Factor Kappa B Signal Pathway.","authors":"Xin Li, Ting Du, Fan Yang, Chun Ge, Chonghe Yang, Lejun Li","doi":"10.4103/ejpi.EJPI-D-24-00101","DOIUrl":"10.4103/ejpi.EJPI-D-24-00101","url":null,"abstract":"<p><strong>Abstract: </strong>This study investigates the mechanism by which a compound mixture of Chuanxiong and Baizhi (CMCB) modulates the TLR4/MyD88/nuclear factor kappa B (NF-κB) pathway to alleviate neuroinflammation in nitroglycerin (NTG)-induced chronic migraine (CM) rat models. In vivo CM rat models were induced with 10 mg/kg NTG, while in vitro models utilized BV2 cells stimulated with lipopolysaccharide. Toxicity of CMCB extracts was assessed through CCK8 assay and lactate dehydrogenase detection. Protein and messenger RNA expression levels were analyzed by quantitative real-time polymerase chain reaction and western blotting. Immunofluorescence was employed to evaluate the nucleoplasmic distribution of NF-κB p65. Inflammatory status and cell apoptosis were evaluated through enzyme-linked immunosorbent assay, flow cytometry, and immunohistochemistry. Results showed that CMCB concentrations below 16 μM were nontoxic to BV2 cells and effectively reduced cell apoptosis and inflammation, akin to the effects of a TLR4 pathway inhibitor, TAK-242. CMCB extracts decreased protein expression of TLR4 and MyD88, phosphorylation of NF-κB p65, and limited NF-κB p65 nuclear translocation. In vivo experiments demonstrated that both zolmitriptan and CMCB treatment ameliorated symptoms like red ear, head scratching, and cage climbing in CM rat models. High dosages of CMCB exhibited comparable efficacy to zolmitriptan in reducing inflammatory responses, indicating that CMCB alleviates neuroinflammation in CM rat models through the inhibition of the TLR4/MyD88/NF-κB signaling pathway.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":"158-167"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144036319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-99 Family of Exosomes Targets Myotubularin-related Protein 3 to Regulate Autophagy in Trophoblast Cells and Influence Insulin Resistance.","authors":"Shao-Xiao Liu, Yang Lv","doi":"10.4103/ejpi.EJPI-D-24-00111","DOIUrl":"10.4103/ejpi.EJPI-D-24-00111","url":null,"abstract":"<p><strong>Abstract: </strong>The global incidence of gestational diabetes mellitus (GDM) continues to rise and is associated with negative outcomes in pregnancy. This study aims to investigate how the miR-99 family of exosomes derived from the placenta targets myotubularin-related protein 3 (MTMR3) to trigger autophagy and alter insulin resistance (IR) in trophoblast cells. In this study, placenta-derived exosomes from plasma samples of patients with GDM and normal pregnant women were isolated to evaluate the expression levels of miR-99 family members (miR-99a, miR-99b, and miR-100) by quantitative real-time polymerase chain reaction. Furthermore, we used Targeted Scan prediction and dual luciferase reporter assays to identify a potential target of the miR-99 family. Finally, Western blotting, CCK8 assay, and glucose level measurement were used to confirm that the miR-99 family regulates autophagy in trophoblast cells through targeting potential targets, thereby affecting IR. Through comprehensive molecular biology techniques, our analysis revealed that, in contrast to normal pregnant women, the placenta-derived exosomes of women with GDM exhibited a significant downregulation of the miR-99 family. Moreover, MTMR3 emerged as a potential target of the miR-99 family, revealing a negative correlation with the levels of miR-99. An increase in MTMR3 expression impaired cellular autophagy and contributed to IR. Conversely, augmenting the miR-99 family can lead to a downregulation of MTMR3, promotion of cellular autophagy, and mitigation of IR. This research demonstrated that the expression of the miR-99 family was reduced in plasma exosomes of GDM. The miR-99 family can directly target MTMR3, leading to its downregulation. This process activated autophagy in trophoblast cells and enhances insulin sensitivity. Consequently, the miR-99 family holds potential as a therapeutic strategy for patients with GDM.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":"176-184"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144056670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Arsenic-induced Diabetic Vascular Diseases through Mitogen-activated Protein Kinase Signaling Pathway: In vitro and In vivo Studies.","authors":"Bi-Yu Liu, Jhih-Syuan Jhu, Man-Lun Syu, Deng-Fwu Hwang","doi":"10.4103/ejpi.EJPI-D-24-00097","DOIUrl":"10.4103/ejpi.EJPI-D-24-00097","url":null,"abstract":"<p><strong>Abstract: </strong>Arsenic (As) is an environmental pollutant that causes endocrine disruption. Diabetes increases the risk of Blackfoot disease, which is a peripheral artery disease caused by chronic exposure to As through drinking water in Taiwan and Bangladesh; however, the mechanism underlying this increased risk remains unclear. Therefore, in this study, we aimed to investigate the mechanisms underlying vascular damage in hyperglycemic conditions caused by As exposure using in vivo and in vitro studies. We utilized an animal model of streptozotocin-induced diabetes that was exposed to As through drinking water for 8 weeks. Subsequently, blood and organ samples of the animals were collected for follow-up analysis. Further, we cultured endothelial cells that were treated with As treatment in glucose condition and detected their biomarkers. The findings revealed that both the diabetes and diabetes + As groups exhibited insulin resistance, weight gain, and increased plasma triglyceride and total cholesterol levels. The diabetes + As group had lower antioxidant activity, which caused the arteries to exhibit prominent luminal narrowing with increased thickness. In vivo study revealed that glucose + As group-induced cell cycle arrest, a 98.80% increase in reactive oxygen species (ROS) levels, and decreased cell viability and mitochondrial membrane potential (MMP). However, in glucose + As group, treatment with SP600125 and U10126 treatment decreased ROS production by 80.5% and 84%, respectively, and restored MMP and cell viability. The glucose-regulated protein 78 level increased in the As as well as glucose + As groups. Our findings demonstrate that As exacerbates vascular damage in individuals with diabetes and its associated complications through the activation of the mitogen-activated protein kinase signaling pathway.</p>","PeriodicalId":519921,"journal":{"name":"Journal of physiological investigation","volume":" ","pages":"127-139"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144049646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}