Naglaa Adly Abd Elazeem, Lamis Abdelghani Salamah, Marwa Abdeltawab Mohammed, Ghada Mahmoud Abd El Aziz, Shaimaa Abd El Tawab Fathi
{"title":"Protective role of vildagliptin against bisphenol-A induced liver injury: targeting oxidative stress, apoptosis, and endoplasmic reticulum stress.","authors":"Naglaa Adly Abd Elazeem, Lamis Abdelghani Salamah, Marwa Abdeltawab Mohammed, Ghada Mahmoud Abd El Aziz, Shaimaa Abd El Tawab Fathi","doi":"10.1080/13813455.2025.2555473","DOIUrl":"https://doi.org/10.1080/13813455.2025.2555473","url":null,"abstract":"<p><p>Bisphenol-A (BPA) is an environmental pollutant that causes hepatic injury. The antioxidant activity of vildagliptin is confirmed. The present study investigated the protective effect of Vildagliptin against BPA-induced hepatotoxicity. Twenty four rats were divided randomly into 4 groups (6 rats/group): A control group, BPA group, BPA + Vildagliptin group and Vildagliptin group. All rats, except the controls were orally administered 30 mg/kg body weight BPA and/or 10 mg/kg Vildagliptin. AST, ALT, Triglycerides and albumin were measured in the serum. MDA, GPX, XBP1, Caspase 3 and BCL2 were measured in liver tissues. BPA group showed a significant decrease of albumin and GPX and a significant increase of triglycerides, AST, ALT and MDA. BPA caused up regulation of caspase3 and XBP1 while caused down regulation of BCL2. The co-administration of Vildagliptin reversed these hazards. The results of this study established the protective effect of Vildagliptin against BPA induced liver dysfunction.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-9"},"PeriodicalIF":2.7,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144991511","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":"Menthol ameliorates thioacetamide-induced renal fibrosis in rats by upregulating SIRT1/Nrf2 and downregulating TGF-β1/Smad3 signalling pathways.","authors":"Elaheh Babaei, Masoumeh Asle-Rousta, Sanaz Mahmazi","doi":"10.1080/13813455.2025.2554677","DOIUrl":"https://doi.org/10.1080/13813455.2025.2554677","url":null,"abstract":"<p><strong>Introduction: </strong>Renal fibrosis is a significant factor in the progression of chronic kidney disease. This study examined how menthol affects thioacetamide (TA)-induced biochemical, molecular, and histopathological damage that leads to renal fibrosis and dysfunction.</p><p><strong>Methods: </strong>Male Wistar rats were treated with TA (200 mg/kg, intraperitoneally) twice a week for four consecutive weeks, along with menthol (10 mg/kg, intraperitoneally) for the same duration.</p><p><strong>Results: </strong>Menthol effectively reduced oxidative stress and inflammation in the kidneys of rats treated with TA. It also lowered the expression of TGF-β1, SMAD3, α-SMA, and KIM-1. Furthermore, menthol prevented the decline in SIRT1 mRNA expression and protein levels while increasing the expression of Nrf2. It inhibited collagen deposition and histological damage in the kidneys and prevented the rise in serum creatinine and BUN levels.</p><p><strong>Conclusion: </strong>Menthol provides protective effects against renal fibrosis induced by thioacetamide. Its antifibrotic effects are mediated by upregulating SIRT1/Nrf2 and downregulating TGF-β1/Smad3 pathways.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-14"},"PeriodicalIF":2.7,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940472","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":"Possible physiological benefits of fasting and exercise.","authors":"Hamed Alizadeh Pahlavani, Ali Veisi","doi":"10.1080/13813455.2025.2550470","DOIUrl":"https://doi.org/10.1080/13813455.2025.2550470","url":null,"abstract":"<p><p>Exercise and fasting, by activating hypothalamic neurons, lead to appetite regulation, increased energy efficiency, increased brown fat cells, and weight loss. Additionally, fasting and exercise affect brain plasticity and cognitive function by reducing oxidative brain damage and increasing brain-derived neurotrophic factor (BDNF), potentially reducing the risk of neurological diseases. In humans, these lifestyle interventions can also modulate autophagy and apoptosis in lymphocytes, especially natural killer (NK) cells, T cells, and B cells, which play an important role in fighting cancer and virus-infected cells. Fasting and exercise increase the concentration of autophagic monocytes, enhance killer T lymphocytes, strengthen the immune system, and delay cancer progression. Fasting and exercise can improve metabolic and inflammatory parameters through immune-related molecules, reducing systemic inflammation. Furthermore, they are associated with changes in the composition and function of gastrointestinal microbes, including an increase in beneficial microbes and a decrease in pathogenic bacteria, along with intestinal epithelial integrity.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-22"},"PeriodicalIF":2.7,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940470","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}
Yosr Z Haffani, Souhaieb Chrigui, Ramla Khiari, Mohamed Bessem Hammami, Sameh Hadj Taieb, Moncef Feki, Rafika Ben Chaouacha-Chekir, Nourhène Boudhrioua
{"title":"Halophyte decocted extract alleviates metabolic and histopathological disturbances induced in human-like rodent model, <i>Psammomys obesus</i>.","authors":"Yosr Z Haffani, Souhaieb Chrigui, Ramla Khiari, Mohamed Bessem Hammami, Sameh Hadj Taieb, Moncef Feki, Rafika Ben Chaouacha-Chekir, Nourhène Boudhrioua","doi":"10.1080/13813455.2025.2541695","DOIUrl":"https://doi.org/10.1080/13813455.2025.2541695","url":null,"abstract":"<p><strong>Background: </strong>The effect of halophyte plant \"Salicornia arabica\" decocted extract (HDE) on histological damage and metabolic disorders induced by a High-Caloric Diet (HCD) in Psammomys obesus (P. obesus) was investigated.</p><p><strong>Methods: </strong>Forty P. obesus were divided into two groups: receiving a natural Low-Caloric Diet (LCD) or a high-caloric diet (HCD). On day 90, each group was further subdivided into two groups, with or without a daily oral administration of HDE at 300 mg/kg body weight for one month. Body weight, glycaemia, and serum lipid profile were assessed. Histopathological analyses on retinal, pancreatic, renal, and adipose tissues were conducted on day 120.</p><p><strong>Results: </strong>HDE administration markedly alleviates the HCD-induced metabolic disorder and histopathological alterations, restoring tissue integrity compared to the untreated HCD group. ATR-FTIR and micronutrient analyses showed HDE contains antioxidant minerals, soluble dietary fibers, and phenolic compounds likely responsible for its effects.</p><p><strong>Conclusion: </strong>HDE may protect against HCD-induced metabolic disorders and tissues alteration in <i>P. obesus</i>.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-16"},"PeriodicalIF":2.7,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144940382","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":"ShQDFHNet: Shepard quantum dilated forward harmonic net for brain tumour detection using MRI image.","authors":"G V Sam Kumar, Rajesh Kumar T","doi":"10.1080/13813455.2025.2541700","DOIUrl":"https://doi.org/10.1080/13813455.2025.2541700","url":null,"abstract":"<p><strong>Introduction: </strong>One of today's major health threats is brain tumours, yet current systems focus mainly on diagnostic methods and medical imaging to understand them. Here, the Shepard Quantum Dilated Forward Harmonic Net (ShQDFHNet) is developed for brain tumour detection using MRI scans.</p><p><strong>Methods: </strong>It starts by enhancing images with high boost filtering to highlight key features, then uses Log-Cosh Point-Wise Pyramid Attention Network (Log-Cosh PPANet) for accurate tumour segmentation, guided by a refined Log-Cosh Dice Loss. To capture texture details, features like Spatial Grey-Level Dependence Matrix (SGLDM) and Gray-Level Co-occurrence Matrix (GLCM) are extracted. The final detection uses ShQDFHNet, combining Shepard Convolutional Neural Network (ShCNN) and Quantum Dilated Convolutional Neural Network (QDCNN), with layers enhanced by a Forward Harmonic Analysis Network.</p><p><strong>Results: </strong>ShQDFHNet achieved strong performance on the Brain Tumour MRI dataset, with 90.69% accuracy, 91.14% True Positive Rate (TPR), and 90.61% True Negative Rate (TNR) using K-fold of 9.</p><p><strong>Discussion: </strong>The use of high boost filtering, Log-Cosh PPANet, and texture-based features improves the input data quality and enables accurate tumor segmentation in MRI scans. The proposed ShQDFHNet model improves feature learning and achieves strong performance on brain tumor MRI data.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-22"},"PeriodicalIF":2.7,"publicationDate":"2025-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871117","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}
Mohamed J Saadh, Tamara Nazar Saeed, Ali Fawzi Al-Hussainy, Ashishkumar Kyada, Suhas Ballal, Mayank Kundlas, A Sabarivani, Jasur Rizaev, Sada Ghalib Taher, Mariem Alwan, Mahmood Jawad, Hiba Mushtaq
{"title":"Mechanistic insights into ubiquinone Q10 in Parkinson's disease: mitochondrial protection, ferroptosis inhibition, and antioxidant recycling.","authors":"Mohamed J Saadh, Tamara Nazar Saeed, Ali Fawzi Al-Hussainy, Ashishkumar Kyada, Suhas Ballal, Mayank Kundlas, A Sabarivani, Jasur Rizaev, Sada Ghalib Taher, Mariem Alwan, Mahmood Jawad, Hiba Mushtaq","doi":"10.1080/13813455.2025.2541698","DOIUrl":"https://doi.org/10.1080/13813455.2025.2541698","url":null,"abstract":"<p><strong>Background: </strong>Parkinson's disease is a progressive neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra. Although the exact cause of Parkinson's disease is still unknown, neuroinflammation and mitochondrial dysfunction have been identified as essential factors in the disease's pathophysiology.</p><p><strong>Methods: </strong>Coenzyme Q10 has gathered considerable attention as a potential therapeutic agent due to its dual function in antioxidant defense and mitochondrial bioenergetics. It is an essential electron carrier in the mitochondrial electron transport chain and plays a crucial role in reducing oxidative stress, a primary cause of neuronal degeneration in Parkinson's disease.</p><p><strong>Results: </strong>Coenzyme Q10 supplements can enhance mitochondrial activity, reduce oxidative stress, and protect dopaminergic neurons from degeneration. To improve Coenzyme Q10 formulations and ascertain its effectiveness in slowing the progression of Parkinson's disease, more study is required.</p><p><strong>Conclusion: </strong>This review examines the neuroprotective mechanisms of Coenzyme Q10 and its potential as a therapeutic option for Parkinson's disease.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-17"},"PeriodicalIF":2.7,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144783356","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":"Correction.","authors":"","doi":"10.1080/13813455.2025.2542631","DOIUrl":"https://doi.org/10.1080/13813455.2025.2542631","url":null,"abstract":"","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-2"},"PeriodicalIF":2.7,"publicationDate":"2025-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144774561","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}
Mohammadreza Bakhoda, Nejat Kheiripour, Keihan Ghatre-Samani, Maryam Akhavan Taheri, Fatemeh Najarzadeh, Mohammad Mehdi Haghighat Lari, Mohammad Esmaeil Shahaboddin
{"title":"Ameliorating the toxicity induced by L-arginine through <i>iris germanica</i> methanolic extract in an experimental model of acute pancreatitis.","authors":"Mohammadreza Bakhoda, Nejat Kheiripour, Keihan Ghatre-Samani, Maryam Akhavan Taheri, Fatemeh Najarzadeh, Mohammad Mehdi Haghighat Lari, Mohammad Esmaeil Shahaboddin","doi":"10.1080/13813455.2025.2541699","DOIUrl":"https://doi.org/10.1080/13813455.2025.2541699","url":null,"abstract":"<p><p>This study evaluates the protective effects of <i>Iris germanica</i> (<i>I. germanica</i>) methanolic extract against L-arginine-induced acute pancreatitis in male rats. The extract's antioxidant potential was confirmed by in vitro assays, revealing 30.76 mg/g of phenolics, 15.86 mg/g of flavonoids, and strong antioxidant activity. HPLC analysis identified catechin and chlorogenic acid as major components. In vivo, rats were divided into five groups: control, L-arginine-only, two <i>I. germanica</i>-treated groups (100 and 400 mg/kg), and a melatonin-treated group. L-arginine elevated serum amylase and lipase levels, while <i>I. germanica</i> extract significantly reduced them, particularly at 24 hours post-treatment. The extract also increased total antioxidant capacity and reduced malondialdehyde and myeloperoxidase levels dose-dependently. Histological analysis showed decreased pancreatic necrosis and edema in treated groups. However, no significant differences were found in cytokine levels (TNF-α, IL-6, IL-10). These findings suggest I. germanica extract may alleviate acute pancreatitis primarily through antioxidant mechanisms.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-17"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144759014","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}
Mohammad-Sadegh Lotfi, Hamidreza Jamali, Fatemeh B Rassouli
{"title":"Network pharmacology and <i>in silico</i> study of quercetin and structurally similar flavonoids as osteogenesis inducers that interact with oestrogen receptors.","authors":"Mohammad-Sadegh Lotfi, Hamidreza Jamali, Fatemeh B Rassouli","doi":"10.1080/13813455.2025.2483910","DOIUrl":"10.1080/13813455.2025.2483910","url":null,"abstract":"<p><strong>Background: </strong>Osteoporosis poses a global health challenge, particularly with an ageing population. Quercetin, isorhamnetin, avicularin, isoquercetin, quercitrin, and taxifolin are natural flavonoids with similar structure that induce ontogenesis.</p><p><strong>Methods: </strong>In the present study, proteins in oestrogen signalling and bone morphogenesis were analysed, and hub genes were identified with Cytoscape, followed by pathway analysis. Then, molecular targets of flavonoids and osteoporosis-related targets were identified, and overlaps were detected. Molecular docking and dynamics simulations assessed flavonoid interactions with ERs.</p><p><strong>Results: </strong>The study identified 14 gene products linked to osteoporosis, including ESR1 and ESR2. Enrichment analyses confirmed ESR involvement in various biological processes. SwissTargetPrediction highlighted quercetin and isorhamnetin as favourable targets for ESR1 and ESR2. Molecular docking and dynamics revealed favourable and stable binding of flavonoids to ERα and ERβ.</p><p><strong>Conclusio: </strong>These interactions suggest therapeutic potential of natural flavonoids for osteoporosis treatment by targeting ERs, laying a foundation for future research in preclinical and clinical settings.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"658-669"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143750877","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":"Anti-atherogenic properties of <i>Plectranthus glandulosus</i> Hook. F. (Lamiaceae) leaves through lipid profile regulation, oxidative stress reduction, and aorta media thickening attenuation in high-fat diet-fed Sprague-Dawley rats.","authors":"Djamila Zouheira, Anu Kajal, Moïse Legentil Nchouwet, Sylviane Laure Poualeu Kamani, Lauve Rachel Tchokouaha Yamthe, Gabriel Agbor Agbor, Sylvie Lea Wansi Ngnokam, Randhir Singh","doi":"10.1080/13813455.2025.2476644","DOIUrl":"10.1080/13813455.2025.2476644","url":null,"abstract":"<p><p>This study investigated the anti-atherogenic effects of <i>Plectranthus glandulosus</i> leaves aqueous, hydro-ethanolic extracts, and ethyl acetate fraction at doses of 100, 200, and 400 mg/kg for 21 d. As results, at the dose of 400 mg/kg, the ethyl acetate fraction significantly (<i>p</i> < .001) decreased the level of total cholesterol (112.52 ± 1.21 mg/dL), triglyceride (76.47 ± 0.97 mg/dL), and LDL-C (22.01 ± 2.92 mg/dL). Whereas, a significant (<i>p</i> < .001) increase was observed in the level of HDL-C (74.97 ± 1.99 mg/dL). Moreover, the atherogenic index significantly (<i>p</i> < .001) decreased (0.008 ± 0.00 mg/dL), while the percentage of atherogenic protection increased (99.13 ± 0.78%). The activity of antioxidant enzymes increased significantly (<i>p</i> < .001), while malondialdehyde concentration decreased. The thickening of aorta media (67.27 ± 7.15 µm) was also attenuated significantly (<i>p</i> < .001). Thus, our finding supports the use of <i>Plectranthus glandulosus</i> for future atherosclerosis drug discovery.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"621-635"},"PeriodicalIF":2.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143622990","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}