Archives of Physiology and Biochemistry最新文献

{"title":"The role of coenzyme Q10 in exercise tolerance and muscle strength.","authors":"Zhenwu Bian, Liu Wei","doi":"10.1080/13813455.2025.2507746","DOIUrl":"https://doi.org/10.1080/13813455.2025.2507746","url":null,"abstract":"<p><p><b>Context</b>: Coenzyme Q10 (CoQ10) is a vital compound found in nearly all cells, and in mitochondria, it facilitates ATP production, and its reduced form acts as a powerful antioxidant, neutralizing reactive oxygen species (ROS) and preventing oxidative damage. Notably, during intense or endurance exercise, the body's increased energy demands and ROS production can lead to oxidative stress, muscle fatigue, inflammation, and exercise-induced muscle damage (EIMD).</p><p><p><b>Objectives</b>: This review will explore the mechanisms of CoQ10, its impact on exercise performance to be addressed.</p><p><p><b>Results</b>: CoQ10 has been shown to counteract these effects by supporting mitochondrial function, cell membranes, and reducing ROS. Research has demonstrated that CoQ10 supplementation lowers lipid peroxidation, reduces muscle damage indicators like creatine kinase (CK), lactate dehydrogenase (LDH-5 or LDH M), and myoglobin (Mb), and accelerates recovery from EIMD. Nevertheless, the impact of CoQ10 on performance has varied depending on factors such as dosage, duration, exercise type, and individual characteristics.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-20"},"PeriodicalIF":2.5,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144135971","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 leptin and leptin receptor gene polymorphisms in bipolar disorder: focus on depressive episodes with atypical features.","authors":"Hasan Mervan Aytac, Yasemin Oyaci, Eren Aytac, Mustafa Pehlivan, Furkan Bahadir Alptekin, Sacide Pehlivan","doi":"10.1080/13813455.2025.2507751","DOIUrl":"https://doi.org/10.1080/13813455.2025.2507751","url":null,"abstract":"<p><p><b>Objective</b>: Our study aims to examine the effect of leptin (<i>LEP</i>) (-2548 G > A) (rs7799039) and leptin receptor (<i>LEPR</i>) (668 A > G) (rs1137101) gene polymorphisms on the etiopathogenesis of bipolar disorder (BD) by comparing them with a control group, as well as their association with depressive episodes featuring atypical symptoms.</p><p><p><b>Methods</b>: The study included a sample of 103 individuals with BD and 103 healthy volunteers. Gene polymorphisms were identified from DNA samples through polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).</p><p><p><b>Results</b>: The distribution of <i>LEPR</i> genotypes was significantly different between BD patients and healthy controls. Specifically, the homozygous <i>LEPR</i> GG genotype was more common in the control group than in BD patients. Additionally, genotype frequency distributions among BD patients varied significantly based on the presence of atypical depressive episodes. The <i>LEPR</i> AA and <i>LEP</i> GG genotypes were significantly more common among patients with a history of atypical depression. Logistic regression showed that the <i>LEP</i> polymorphism and Hamilton Depression Rating Scale (HAM-D) score predict atypical depression in BD.</p><p><p><b>Conclusion</b>: In summary, while the <i>LEPR</i> polymorphism is linked to BD, the <i>LEP</i> polymorphism and symptom severity appear to predict atypical depressive episodes.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-9"},"PeriodicalIF":2.5,"publicationDate":"2025-05-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126474","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":"The antioxidant and anti-inflammatory effects of gallic acid and/or cerium oxide nanoparticles synthesized by gamma-irradiation ameliorate cisplatin-induced hepatic injury.","authors":"Mostafa Saif-Elnasr, Alshimaa M Elmalawany, Assmaa Fathi Abdel-Khalek","doi":"10.1080/13813455.2025.2507760","DOIUrl":"https://doi.org/10.1080/13813455.2025.2507760","url":null,"abstract":"<p><strong>Context: </strong>Cisplatin is a widely utilised chemotherapeutic agent for cancer therapy, but various systemic toxicities limit its effectiveness.</p><p><strong>Objective: </strong>This study aimed to assess the hepatoprotective properties expressed by gallic acid (GA) and gamma-irradiation synthesized cerium oxide nanoparticles (CONPs) in response to hepatic damage produced by cisplatin in albino rats.</p><p><strong>Materials and methods: </strong>Serum AST and ALT activities and levels of MDA, TAC, NF‑kB, TNF‑α, and TGF‑β were determined in hepatic tissue, along with histopathological examination.</p><p><strong>Results: </strong>The executive impact of cisplatin led to a notable rise in the serum activity of hepatic enzymes AST and ALT. Conversely, in the groups receiving treatment with either or both GA and CONPs, the liver function enzymes exhibited a decline in their activity. In addition, in the hepatotoxicity models, the levels of hepatic MDA were significantly increased, accompanied by a reduction of hepatic TAC. While administration of GA, CONPs or their combination to cisplatin-injected rats resulted in a noteworthy reduction in MDA level. Conversely, the hepatic TAC level increased compared to the group that received cisplatin. The hepatic tissue architecture in rats exposed to cisplatin was found to undergo significant alterations. Furthermore, the cisplatin induced overexpression of NF-kB, TNF-α, and TGF-β. The hepatic histopathological changes observed in rats induced with cisplatin were significantly attenuated after pre-treatment with GA, CONPs, and their combination. GA, CONPs, and their co-administration resulted in reducing the levels of NF-κB, TNF-α and TGF-β compared to the group received cisplatin.</p><p><strong>Discussion and conclusion: </strong>In summary, GA and CONPs synthesized by gamma-irradiation resulted in a noteworthy reduction of liver damage caused by cisplatin exposure. Their potent antioxidant and immunoprotective properties were cited as the cause of this phenomenon.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-13"},"PeriodicalIF":2.5,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144126476","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":"https://doi.org/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":"1-12"},"PeriodicalIF":2.5,"publicationDate":"2025-05-21","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":"The impact of a multi-species probiotic supplementation on clinical symptoms and biochemical factors in patients with irritable bowel syndrome: a randomised controlled trial.","authors":"Shirin Hajiani, Maryam Tajabadi Ebrahimi, Amir Sadeghi, Nakisa Zarrabi Ahrabi, Abbas Yadegar","doi":"10.1080/13813455.2025.2507749","DOIUrl":"https://doi.org/10.1080/13813455.2025.2507749","url":null,"abstract":"<p><p><b>Background:</b> Intestinal inflammation and oxidative stress contribute to the pathophysiology of irritable bowel syndrome (IBS). This clinical trial investigated the effects of a probiotic supplementation on symptom severity and quality of life (QOL) in IBS patients.</p><p><p><b>Methods:</b> Forty-six IBS patients were randomised to receive either a multi-species probiotic or placebo for 8 weeks. Clinical symptoms were evaluated using the IBS Severity Scoring System (IBS-SSS) and IBS QOL questionnaire. Serum levels of IFN-γ, IL-1β, IL-10, IL-6, malondialdehyde (MDA), total antioxidant capacity (TAC), and nitric oxide (NO) were measured before and after the intervention.</p><p><p><b>Results:</b> After 8 weeks, the probiotic group showed significant improvements in QOL scores, and reductions in IBS-SSS and MDA levels compared to placebo group. TAC levels were significantly higher in probiotic group. However, no significant differences were observed in cytokine or NO levels.</p><p><p><b>Conclusions:</b> This multi-species probiotic supplement was safe and effective in reducing symptom severity and improved QOL of IBS patients.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-11"},"PeriodicalIF":2.5,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144109115","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":"Comparable hepatocellular metabolomic signatures under glucose and palmitic acid treatment relative to butyrate in relation to metabolic dysfunction-associated fatty liver disease.","authors":"Priyankar Dey","doi":"10.1080/13813455.2025.2500651","DOIUrl":"https://doi.org/10.1080/13813455.2025.2500651","url":null,"abstract":"<p><strong>Introduction: </strong>Among the dietary factors, glucose, and fatty acids are known to trigger fatty liver disease, while butyrate attenuates steatosis.</p><p><strong>Objective: </strong>To decipher the hepatocellular altered metabolome under nutrient perturbation relevant to fatty liver disease.</p><p><strong>Methods: </strong>HepG2 cells were cultured under the influence of sub-lethal doses of glucose, palmitic acid (PA), and butyrate. Following the treatment, intracellular metabolites were extracted and derivatized for GCMS analysis. Chemical class enrichment, metabolic pathway analysis, and metabolomic interactome analysis were undertaken.</p><p><strong>Results: </strong>Glucose, PA and butyrate caused loss of cell viability at 160 mM, 1600 µM, and 40 mM concentration, respectively. A total of 39, 47, 52, and 51 metabolites were identified in control, glucose, PA, and butyrate, respectively, among which 2-ethylhexanoic acid in control and 2-ethylhexan-1-ol in glucose, PA and butyrate were the most abundant metabolites. Pathways related to the mitochondrial electron transport chain were highly enriched in glucose and PA treatments, leading to increased free radicals. The metabolites identified under glucose and PA treatment were linked to the metabolomic markers of metabolic liver diseases.</p><p><strong>Conclusion: </strong>Our data showed that the hepatocellular metabolome of HepG2 cells under glucose and PA treatment is closely related, while the metabolome and pathways associated with butyrate treatment are associated with energy metabolism and alleviation of fatty liver.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-11"},"PeriodicalIF":2.5,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075757","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":"Heptaminol-induced metabolic liver and cardiac injuries in rats: phytochemical screening, experimental, computational modelling and pharmacological study of <i>phoenix dactylifera</i> seeds.","authors":"Raoudha Abbassi, Hafsia Bouzenna, Riadh Badraoui, Mohammad Atwan, Faten Brahmi, Anouer Feriani, Arif J Siddiqui, Mohd Adnan, Ahmed Mohajja, Sirine Choura, Mohamed Chamkha, Najla Hfaiedh","doi":"10.1080/13813455.2025.2504169","DOIUrl":"https://doi.org/10.1080/13813455.2025.2504169","url":null,"abstract":"<p><p><b>Introduction:</b> Heptaminol (HEP) is widely used and characterized by liver and cardiac risk factors, dysregulated prooxidant-antioxidant balance, and inflammation. This study aimed to study the phytochemical composition of date seeds of <i>Phoenix dactylifera</i> (DSPE) by GC-MS analysis and to assess the <i>in vitro</i> antioxidant, anticoagulant and ACE activities.</p><p><p><b>Methods:</b> The hepato and cardiotoprotective effect against HEP-induced toxicity in rats have been assessed using biochemical, histological and computational assays.</p><p><p><b>Results:</b> HEP increased the body weight, associated significant increases in total cholesterol, triglycerides, total and direct bilirubin, alkaline phosphatase, creatinine kinase-MB, ACE, and troponin-T, exhibited changes in ECG pattern, including ST-segment elevation, and increased rate of TBARS with decreases in the antioxidant enzymatic. DSPE improved these biomarkers alterations through anti-oxidative and anti-coagulant activities, which were confirmed by histopathological examinations. The computational findings supported the in vivo results and showed that DSPE compounds bound Hypoxia-Inducible Factor (HIF-1α) and Insulin-Like Growth Factor (IGF1) with acceptable affinities and molecular interactions.</p><p><p><b>Conclusion:</b> DSPE had hepato and cardioprotective effects against HEP-induced heart and liver injuries. DSPE can be used to prevent acute thrombosis due to its different bioactive compounds.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-15"},"PeriodicalIF":2.5,"publicationDate":"2025-05-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075758","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":"https://doi.org/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":"1-13"},"PeriodicalIF":2.5,"publicationDate":"2025-05-14","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":"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":"https://doi.org/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":"1-10"},"PeriodicalIF":2.5,"publicationDate":"2025-05-13","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":"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":"https://doi.org/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":"1-18"},"PeriodicalIF":2.5,"publicationDate":"2025-05-13","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}