Archives of Physiology and Biochemistry最新文献

{"title":"The inhibitory impact of glutathione (GSH) and ascorbic acid (vitamin C) compounds on glucose-6-phosphate dehydrogenase (G6PD) enzyme purified from sheep liver.","authors":"Zehra Bas, Vedat Turkoglu","doi":"10.1080/13813455.2025.2567343","DOIUrl":"https://doi.org/10.1080/13813455.2025.2567343","url":null,"abstract":"<p><strong>Objective: </strong>Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme with many essential biochemical functions. However, in various cancer diseases, increased activity of G6PD causes cancer cells to grow, so G6PD inhibitors have become a significant area of research in cancer treatment.</p><p><strong>Materials and methods: </strong>Here, G6PD was purified 4530-fold with affinity chromatography using 2',5'-ADP Sepharose 4B from sheep liver. The effects of reduced glutathione (GSH) and ascorbic acid (vitamin C) on G6PD activity were explored.</p><p><strong>Results and discussion: </strong>GSH and ascorbic acid showed a significant inhibitory effect on G6PD, and IC₅₀ values were found as 0.37 µM and 34.66 µM, respectively. The inhibition type from Lineweaver-Burk plots of these compounds was identified as non-competitive inhibition. The <i>K_i</i> values of GSH and ascorbic acid were calculated as 0.48 µM and 30.47 µM, respectively.</p><p><strong>Conclusion: </strong>In this study, it was observed that GSH and ascorbic acid antioxidant compounds exhibit an inhibitory effect on G6PD and may be protective and preventive against cancer.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-10"},"PeriodicalIF":2.7,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145237761","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 role of butylated hydroxyanisole (BHA) and hydroxytoluene (BHT) against oxidative stress-induced inflammatory response in carbon tetrachloride-induced acute hepatorenal toxicity.","authors":"Barsha Dassarma, Santanu Kar Mahapatra, Dilip Kumar Nandi, Somnath Gangopadhyay, Saptadip Samanta","doi":"10.1080/13813455.2025.2493105","DOIUrl":"10.1080/13813455.2025.2493105","url":null,"abstract":"<p><strong>Background: </strong>Any toxicity initially damages the hepatic system, followed by renal dysfunction. Previously, it was established that carbon tetrachloride (CCl₄) intoxication severely damaged hepatocytes. Moreover, CCl₄-mediated toxicity significantly impacted immune functions and influenced the inflammatory response, with mitochondrial dysfunction. The present study focused on the levels of inflammatory markers and mitochondrial dysfunction, as well as the protective role of BHA and BHT.</p><p><strong>Methods: </strong>In the present study, hepatorenal dysfunction was developed in experimental rats by applying a subcutaneous injection of CCl₄ with a dose of 230 mg/kg bwt/rat/day. The level of immune toxicity was determined by measuring C-reactive protein (CRP), IL-6, 12, TNF-α, IL-10, and TGF-β in CCl4 intoxicated group and pretreated BHA and BHT groups. ROS generation and MMP were also measured in hepatic and renal cells using flow cytometric technique.</p><p><strong>Results: </strong>The level of toxicity was determined by a significant increase of CRP (407.29%), IL-6 (525.65%), IL-12 (1026.54%), and TNF-α (1007.33%) in CCl₄ intoxicated group, while IL-10 and TGF-β were significantly decreased 84.65% and 66.36%, respectively. CCl₄ intoxication caused decreased mitochondrial membrane potential and high levels of intracellular ROS generation. Pretreatment with BHA (0.5 mg/kg/bwt) and BHT (0.8 mg/kg/bwt) significantly (<i>p</i><0.001, <i>p</i><0.05) reduced inflammatory markers in the CCl4-treated group, restored mitochondrial membrane potential and decreased intracellular ROS levels.</p><p><strong>Conclusion: </strong>BHA and BHT treatment could restrict the higher concentration of pro-inflammatory markers by scavenging ROS. Therefore, the study suggested that supplementation of BHA and BHT could be an alternative treatment for preventing hepatorenal dysfunctions.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"728-735"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143959890","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":"Cholecalciferol alleviates testicular dysfunction in experimental hyperthyroidism via antioxidant, anti-inflammatory and antiapoptotic effects.","authors":"Heba Rady Salem, Hend Ahmed Kasem","doi":"10.1080/13813455.2025.2503479","DOIUrl":"10.1080/13813455.2025.2503479","url":null,"abstract":"<p><strong>Background: </strong>This study aimed to investigate the possible protective effect of cholecalciferol against testicular dysfunction in L-thyroxine-induced hyperthyroid rat model.</p><p><strong>Methods: </strong>Twenty-four adult male rats were divided into three groups: control, hyperthyroid, and hyperthyroid cholecalciferol treated. At the end of four weeks, serum samples were collected for measurement of thyroid hormones, testosterone, and serum inflammatory markers (interleukin-6 and tumour necrosis factor-alpha). Thereafter, malondialdehyde and antioxidant enzymes were assessed in the testicular homogenate. Also, histological and immunohistochemical studies of the testicular tissues were done.</p><p><strong>Results: </strong>The current results showed lower serum testosterone and testes weight in hyperthyroid rats than control group, with significantly elevated serum inflammatory markers, and disturbed oxidant/antioxidant status in the testicular tissues. This was associated with structural abnormalities. Immunohistochemical study showed upregulation of caspase-3 and downregulation of proliferating cell nuclear antigen (PCNA) in hyperthyroid rats. Cholecalciferol supplementation significantly improved the testicular dysfunction and the testicular pathological features in the hyperthyroid rats. It significantly decreased the levels of serum inflammatory markers and malondialdehyde levels. Also, cholecalciferol supplementation increased the activity of the antioxidant enzymes in the testicular tissue, downregulated caspase-3 and upregulated PCNA in the testicular tissues.</p><p><strong>Conclusion: </strong>Cholecalciferol could ameliorate pathophysiological changes in rat testes of hyperthyroid rats.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"840-849"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143953246","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":"Relationship between MTHFR 677C > T polymorphism and serum PIVKA-II levels in hepatocellular carcinoma.","authors":"Hongyu Zhang, Baixiu Wu, Liang Zhang, Zheng Peng","doi":"10.1080/13813455.2025.2493107","DOIUrl":"10.1080/13813455.2025.2493107","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is a major public health problem with increasing incidence and mortality worldwide. The methylenetetrahydrofolate reductase (MTHFR) 677 C > T polymorphism is associated with the development and progression of various tumours, while protein induced by vitamin K absence II (PIVKA-II) is an important tumour marker for the diagnosis of HCC. This study aims to investigate the relationship between the MTHFR 677 C > T polymorphism and serum PIVKA-II levels in HCC patients, providing new insights for early diagnosis, risk assessment, and prognosis evaluation of HCC.</p><p><strong>Methods: </strong>This study included 120 HCC patients and 100 healthy controls. MTHFR 677 C > T genotyping was performed using fluorescent quantitative PCR, and serum PIVKA-II levels were measured. Bioinformatics analysis was used to explore the expression of the MTHFR gene in HCC and its relationship with prognosis.</p><p><strong>Results: </strong>MTHFR 677 C > T TT carriers had an increased risk of HCC (OR = 2.393; 95% CI 1.055-5.429; <i>p</i> = 0.037); the risk of HCC for T gene carriers was 58.3% higher than that for C gene carriers in the allele model (OR = 1.583; 95% CI 1.059-2.364; <i>p</i> = 0.025). The difference in serum PIVKA-II concentration was statistically significant between the controls, stage I-II patients, and stage III-IV patients (<i>p</i> < 0.05), and the difference in serum PIVKA-II concentration was statistically significant between patients with the TT genotype and patients with the CC and CT genotypes (all <i>p</i> values less than 0.05). UALCAN database analysis showed that MTHFR gene expression levels were increased in patients with HCC, and the high expression of the MTHFR gene was negatively correlated with patient survival rates.</p><p><strong>Conclusions: </strong>There is an association between the MTHFR 677 C > T TT genotype and serum PIVKA-II levels in HCC. This could help identify high-risk individuals and assess disease severity, providing a potential genetic biomarker for the diagnosis of HCC.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"736-743"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963154","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":"High-intensity interval training prevents high-fat diet-induced hepatic steatosis by modulating miRNA-34a, miRNA-467b, and their primary target proteins in male rats.","authors":"Amir Mohammad Zobeydi, Mohammad Reza Kordi, Reza Gharakhanlou, Hamidreza Khalounejad, Mohammad Parastesh","doi":"10.1080/13813455.2025.2507306","DOIUrl":"10.1080/13813455.2025.2507306","url":null,"abstract":"<p><strong>Aims: </strong>High-fat diet (HFD) consumption contributes to obesity and liver damage, while exercise training may counteract these effects. Given the regulatory role of microRNAs in lipid metabolism, this study investigates the impact of high-intensity interval training (HIIT) and HFD on hepatic fat accumulation, as well as the expression of miRNA-34a, miRNA-467b, and their associated proteins.</p><p><strong>Main methods: </strong>Twenty-four male rats were randomly assigned to four groups: (1) CON, (2) HIIT, (3) HFD, and (4) HIIT+HFD. The HFD groups received a 60% fat diet, while the rats in the HIIT groups performed high-intensity interval training (3 sessions/week, 2.5 minutes high-intensity running × 90% maximal running capacity (MRC) with 2.5 minutes active rest × 50% MRC, for ten weeks). Forty-eight hours post-intervention, blood and liver samples were collected to assess histopathology, liver enzymes, and the expression of miRNA-34a, miRNA-467b, SIRT1, PPAR-ɑ, and LPL proteins.</p><p><strong>Key findings: </strong>The HFD group exhibited excessive hepatic lipid accumulation, whereas HIIT significantly prevented HFD-induced hepatic steatosis, as confirmed by histopathological examinations. Liver enzyme levels (AST, ALT, and ALP) were significantly higher in the HFD group and significantly lower in both the HIIT and HIIT+HFD groups. Additionally, HIIT significantly increased miRNA-467b, SIRT1, and PPAR-ɑ expression while significantly decreasing miRNA-34a and LPL expression, preventing the effects of HFD.</p><p><strong>Significance: </strong>Our findings identified a novel molecular mechanism confirming that HIIT is beneficial to prevent hepatic steatosis and hepatic damage induced by HFD, likely due to the modulation of miRNA-467b, miRNA-34a, and their main target proteins.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"874-885"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144118618","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":"Insulin- and glucagon-producing cells in the liver and biliary-pancreatic axis of rats with experimentally induced metabolic syndrome.","authors":"M Gulubova, A Tolekova, D Berbatov, I Stefanov, D Chonov, N Aydoglu","doi":"10.1080/13813455.2025.2503482","DOIUrl":"10.1080/13813455.2025.2503482","url":null,"abstract":"<p><strong>Context: </strong>The generation of insulin-producing cells (IPCs) as cell replacement therapy for diabetes treatment is challenging.</p><p><strong>Objective: </strong>We have evaluated the presence of insulin-positive (insulin⁺) and glucagon-positive (glucagon⁺) cells in hepatocytes, peribiliary glands (PBGs), and liver sinusoidal endothelial cells (LSECs).</p><p><strong>Materials and methods: </strong>Wistar rats are subjected to a diet including administration of 15% fructose solution for 3 months. Tissue samples are processed for immunohistochemistry with antibodies against insulin, glucagon, ghrelin, somatostatin, PDX1, and SOX9. Blood glucose levels and lipid profile are investigated.</p><p><strong>Results: </strong>In treated rats, Ins⁺ and glucagon⁺ hepatocytes are found around central veins. In PBGs, Ins⁺ and glucagon⁺ endocrine cells (ECs) are detected. LSECs show insulin⁺ and glucagon⁺ cellular membranes. The nuclei of LSECs in treated rats are SOX9-positive.</p><p><strong>Conclusions: </strong>Our experiment of fructose-induced metabolic syndrome shows the appearance of Ins⁺ and glucagon⁺ ECs in extrahepatic biliary pathways and hepatocytes. Interestingly, SOX9⁺ nuclei of LSECs are observed.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"850-858"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144526266","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":"Meteorin-like protein (Metrnl): a key exerkine in exercise-mediated cardiovascular health.","authors":"Hamid Alizadeh, Ahmad Parsaeifar, Roohollah Mohammadi Mirzaei","doi":"10.1080/13813455.2025.2497272","DOIUrl":"10.1080/13813455.2025.2497272","url":null,"abstract":"<p><strong>Context: </strong>Cardiovascular diseases (CVDs) remain a leading global cause of mortality, necessitating non‑pharmacological interventions such as exercise. Meteorin‑like protein (Metrnl), an exercise‑induced myokine and adipokine, has emerged as a critical mediator of exercise‑mediated cardiovascular benefits, though its specific mechanisms and clinical implications remain underexplored.</p><p><strong>Objective: </strong>This review synthesizes current evidence on Metrnl's role as a key exerkine in cardiovascular health, focusing on its exercise‑induced regulatory mechanisms, tissue‑specific effects, and therapeutic potential for CVD management.</p><p><strong>Methods: </strong>A comprehensive analysis of preclinical and clinical studies was conducted, encompassing molecular, metabolic, and anti‑inflammatory pathways linked to Metrnl. Literature from PubMed, Scopus, and Web of Science was systematically reviewed to evaluate Metrnl's role in exercise‑mediated cardiovascular adaptations.</p><p><strong>Results: </strong>Exercise‑induced Metrnl enhances endothelial function, vascular remodeling, and metabolic regulation via AMPK, PPARγ, and KIT receptor signaling. It promotes glucose/lipid metabolism, angiogenesis, and anti‑inflammatory responses, reducing atherosclerotic risks and improving cardiac repair post‑infarction. Clinically, Metrnl levels correlate with CVD severity, acting as a biomarker for risk stratification. Acute exercise elevates Metrnl, while chronic training effects vary by modality and population. Paradoxically, elevated plasma Metrnl in acute cardiac events predicts adverse outcomes, whereas reduced levels in chronic conditions (e.g., diabetes, heart failure) reflect metabolic dysregulation.</p><p><strong>Discussion: </strong>Metrnl bridges exercise benefits to cardiovascular health through inter‑organ crosstalk, yet discrepancies exist in its chronic exercise‑mediated regulation. Its dual role as a protective mediator and stress‑responsive biomarker underscores context‑dependent interpretations. Unresolved questions include receptor specificity, tissue autonomy, and therapeutic delivery strategies.</p><p><strong>Conclusion: </strong>Metrnl is a pivotal exerkine with promising diagnostic and therapeutic potential for CVDs. Translating its exercise‑mediated benefits into clinical applications requires further human trials to validate mechanisms and optimize interventions. Harnessing Metrnl could revolutionize strategies for CVD prevention and rehabilitation, leveraging exercise's molecular advantages.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"713-727"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966131","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":"Selenium deficiency modulates neonatal pulmonary alveolar development via mitochondrial ROS accumulation and oxidative stress mediated by STAT3 inhibition.","authors":"Hong-Yan Tan, Yao-Lin Xiang, Mei-Juan Tan, Chao-Ce Fang, Ya-Ping Zhang, Fen Peng","doi":"10.1080/13813455.2025.2502451","DOIUrl":"10.1080/13813455.2025.2502451","url":null,"abstract":"<p><p><b>Context</b>: Recent findings suggest that Selenium (Se) deficiency in neonates may hinder pulmonary alveolar development, but the underlying molecular mechanisms remain underexplored.</p><p><p><b>Objective</b>: This study utilised a neonatal mouse model to investigate the effects of dietary Se deficiency on pulmonary alveolar development.</p><p><p><b>Materials and methods</b>: Techniques such as quantitative PCR, Western blotting, and immunohistochemistry were employed to assess gene and protein expression related to alveolar development and oxidative stress markers. Mitochondrial ROS accumulation was quantified using MitoSOX staining, and the activity of sirtuin 3 (STAT3), a key transcription factor involved in oxidative stress responses, was analysed.</p><p><p><b>Results</b>: Our findings indicate that Se-deficient neonates exhibit significantly impaired alveolar development characterised by reduced alveolar number and surface area. These structural alterations were associated with increased mitochondrial ROS levels and oxidative stress. Furthermore, Se deficiency resulted in decreased STAT3 phosphorylation, suggesting a mechanism whereby Se influences alveolar development through modulation of STAT3 activity and mitochondrial function.</p><p><p><b>Discussion and conclusion</b>: Se plays a critical role in neonatal pulmonary development by modulating oxidative stress and mitochondrial dynamics via the STAT3 pathway. The study underscores the potential of Se supplementation as a strategic intervention to promote alveolar maturation and prevent pulmonary disorders in neonates. Further research is recommended to explore the therapeutic thresholds and timing of Se administration to optimize pulmonary outcomes.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"792-804"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075759","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":"Evaluation of <i>Annona muricata</i> for hepatoprotection, hematological assessment and inhibitor of TGFβR1 in liver diseases.","authors":"Zacchaeus S Ololade, Iyadunni A Anuoluwa, Olayinka F Onifade, Adewumi I Adeagbo, Olawumi T Oyebanji, Ademola O Asaju, John C Eze","doi":"10.1080/13813455.2025.2499840","DOIUrl":"10.1080/13813455.2025.2499840","url":null,"abstract":"<p><strong>Background: </strong>This study was conducted to assess the hepatoprotective potential of Annona muricata flower (AMF) using albino rats' model.</p><p><strong>Materials and methods: </strong>Liver function assays such as alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin (TBILI), antioxidants, haematology (HGB), histology, inhibition of transforming growth factor beta receptor I (TGFβR1) and antibacterial assays were investigated.</p><p><strong>Results and discussion: </strong>Induction with acetaminophen gave rise to a significant increase (p < 0.05) in serum of liver enzymes of ALT, AST, ALP and TBILI in the acetaminophen (APAP) only group, which indicates hepatocellular injury, whereas AMF attenuated liver enzymes level. The histological assessment confirmed that AMF possesses blood-enhancing ability. AMF significantly showed inhibition of TGFβR1. AMF was active against all the tested bacteria with high zones of inhibition.</p><p><strong>Conclusion: </strong>This study provides information on the uses of AMF as a natural product for hepatoprotection and other therapeutic purposes.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"763-780"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143960041","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 effects of <i>Cuscuta chinensis</i> Lam. extract against learning and memory dysfunction induced by streptozotocin and amyloid β_25-35 <i>in vivo</i> model.","authors":"Ji-Hyun Kim, Hyo Jeong Seo, Byeong Wook Noh, Mei Tong He, Yung-Hyun Choi, Eun Ju Cho, Jeong Sook Noh","doi":"10.1080/13813455.2025.2502861","DOIUrl":"10.1080/13813455.2025.2502861","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is associated with hyperglycaemia and amyloid beta (Aβ) accumulation. In the present study, we investigated whether an aqueous extract of <i>Cuscuta chinensis</i> Lam. (CCWE) improved cognitive disorder in a hyperglycaemic and cognitive-impaired mouse model. Hyperglycaemia was induced by streptozotocin (STZ, 50 mg/kg) and a single intracerebroventricular injection of Aβ_25-35 (25 nM) was performed. The Aβ_25-35-injected hyperglycaemic mice were then administered CCWE (100 or 200 mg/kg/day) for 14-d. The protective effects of the CCWE were evaluated by behavioural tests and western blot analysis. The bioactive compounds in CCWE were isolated by UPLC-QTOF/MS analysis. The administration of CCWE improved the learning and memory function in STZ/Aβ_25-35-injected mice. Moreover, CCWE positively regulated the amyloidogenic pathway-related proteins and insulin signalling-related proteins. The bioactive components in CCWE were also identified. These findings suggest the possibility of CCWE as a potential candidate for the dual-targeting treatment of hyperglycaemia and AD.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"805-817"},"PeriodicalIF":2.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964563","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}