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Archives Of Physiology And Biochemistry[JOURNAL]

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Ellagic acid protects against gastric ulcer in male rats by antioxidant and anti-inflammatory mechanisms: modulation of NF-κβ/COX-2 and Nrf2/HO-1 pathways.

Eldesoqui M, Albadawi EA, Dawood AF … +10 more , Soliman RHM, Ahmed HS, Saeed ZM, Elwany NE, Ashour WMR, Elshafey M, Al-Haider SM, Abdelghany EMA, El-Mansi AA, Ali SK

Arch Physiol Biochem · 2025 Dec · PMID 40620128 · Publisher ↗

BACKGROUND: Gastric ulcer is commonly affected by several causes, including stress. This work examined the gastroprotective effects of ellagic acid (EA), in stress-induced gastric ulcers in Wistar rats. METHODS: Forty ma... BACKGROUND: Gastric ulcer is commonly affected by several causes, including stress. This work examined the gastroprotective effects of ellagic acid (EA), in stress-induced gastric ulcers in Wistar rats. METHODS: Forty male Wistar rats were categorized into five groups: a normal control group, a stress-induced ulcer group, and three groups receiving EA treatment (5 mg, 10 mg, and 20 mg). Gastric ulcers were elicited using a water immersion stress model. Macroscopic and histological assessments, together with biochemical immunohistochemical studies were performed. RESULTS: EA therapy markedly decreased ulcer scores and indices in a dose-dependent manner. EA decreased TNF-α, IL-1β and MDA and augmented PGE1 and GSH. Histopathological assessments verified the results. The immunohistochemical analysis revealed increased Nrf2 and HO-1 levels and decreased NF-κB and COX-2 levels in the EA-treated groups. CONCLUSION: EA demonstrates gastroprotective properties against stress-induced gastric ulcers via its anti-inflammatory and antioxidant mechanisms in a dose-dependent manner.

Unveiling the mechanism of Coenzyme Q10 in ameliorating ageing related oxidative and inflammatory lung alterations in rats targeting PI3K/AKT/Nrf-2 signaling pathway.

Abdel-Hakeem EA, D M Toni N, Mohamed Elroby Ali D … +2 more , Marey H, A Abdel-Hamid H

Arch Physiol Biochem · 2025 Dec · PMID 40591854 · Publisher ↗

: Lung is one of the vital organs that is affected by the ageing process. Searching for natural antioxidants is mandatory to boost healthier longevity. Accordingly, we sought to explore the probable protective effect of... : Lung is one of the vital organs that is affected by the ageing process. Searching for natural antioxidants is mandatory to boost healthier longevity. Accordingly, we sought to explore the probable protective effect of Coenzyme Q10 (Q10) on experimentally induced lung ageing and study the supposed involved mechanistic pathways. : Rats were allocated into groups; control, D-galactose (D-gal), D-gal + Q10 and D-gal + Q10+ LY294002 (LY; phosphatidylinositol 3-kinases (PI3K)/protein kinase B (AKT) inhibitor). Sera and lung tissues were gathered for evaluating markers of oxidative stress, inflammation, fibrosis, and cell senescence by different methods.Immunohistochemistry for senescence associated beta galactosidase (SA-βGal), Capsase-3, and P53 were also evaluated. : Induction of lung ageing resulted in deleterious lung alterations which were ameliorated by Q10; however, its protective effect was abolished by co-administration of LY. : Q10 secured the lung against the ageing process its antioxidant, anti-inflammatory, and anti-apoptotic effects through the activation of the PI3K/AKT/Nrf-2 pathway.

An efficient attention Densenet with LSTM for lung disease detection and classification using X-ray images supported by adaptive R2-Unet-based image segmentation.

Betha SK, Dev DR, Sunkara K … +2 more , Kodavanti PV, Putta A

Arch Physiol Biochem · 2025 Dec · PMID 40590298 · Publisher ↗

Lung diseases represent one of the most prevalent health challenges globally, necessitating accurate diagnosis to improve patient outcomes. This work presents a novel deep learning-aided lung disease classification frame... Lung diseases represent one of the most prevalent health challenges globally, necessitating accurate diagnosis to improve patient outcomes. This work presents a novel deep learning-aided lung disease classification framework comprising three key phases: image acquisition, segmentation, and classification. Initially, chest X-ray images are taken from standard datasets. The lung regions are segmented using an Adaptive Recurrent Residual U-Net (AR2-UNet), whose parameters are optimised using Enhanced Pufferfish Optimisation Algorithm (EPOA) to enhance segmentation accuracy. The segmented images are processed using "Attention-based Densenet with Long Short Term Memory(ADNet-LSTM)" for robust categorisation. Investigational results demonstrate that the proposed model achieves the highest classification accuracy of 93.92%, significantly outperforming several baseline models including ResNet with 90.77%, Inception with 89.55%, DenseNet with 89.66%, and "Long Short Term Memory (LSTM)" with 91.79%. Thus, the proposed framework offers a dependable and efficient solution for lung disease detection, supporting clinicians in early and accurate diagnosis.

Insulin- and glucagon-producing cells in the liver and biliary-pancreatic axis of rats with experimentally induced metabolic syndrome.

Gulubova M, Tolekova A, Berbatov D … +3 more , Stefanov I, Chonov D, Aydoglu N

Arch Physiol Biochem · 2025 Oct · PMID 40580069 · Publisher ↗

CONTEXT: The generation of insulin-producing cells (IPCs) as cell replacement therapy for diabetes treatment is challenging. OBJECTIVE: We have evaluated the presence of insulin-positive (insulin) and glucagon-positive (... CONTEXT: The generation of insulin-producing cells (IPCs) as cell replacement therapy for diabetes treatment is challenging. OBJECTIVE: 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). MATERIALS AND METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Dysregulation of the glycoprotein zymogen granules in pancreatic acinar cells in acute pancreatitis: differential protection by vitamin E and metformin.

Al Amri FS, Alzamil NM, Al-Ani B … +7 more , Zafrah H, Bayoumy NM, Abd Ellatif M, Kamar SS, Alqahtani SM, Omar AI, ShamsEldeen AM

Arch Physiol Biochem · 2025 Dec · PMID 40523046 · Publisher ↗

We investigated whether induction of acute pancreatitis (AP) can cause dysregulation in the glycoprotein zymogens, following episodes of nitrosative stress, which may be differentially protected by vitamin E and metformi... We investigated whether induction of acute pancreatitis (AP) can cause dysregulation in the glycoprotein zymogens, following episodes of nitrosative stress, which may be differentially protected by vitamin E and metformin. AP was induced in rats by L-arginine (2.5 g/kg) injections (two doses given at 1-h interval). The protective groups were pre-treated with either vitamin E (60 mg/kg) or metformin (50 mg/kg) prior to L-arginine injections and continued on these medications until being sacrificed. AP markedly decreased the density of zymogen granules in pancreatic acinar cells (44.5 ± 2.2% in control versus 9.2 ± 1.9% in AP), alongside tissue damage and a significant ( < 0.0001) increase in biomarkers of nitrosative stress (iNOS), inflammation (IL-6 and TNF-α mRNA), and pancreatic injury (amylase, lipase, LDH, and MPO). All these parameters were significantly ( ≤ 0.0005) protected by vitamin E and metformin, with vitamin E providing greater protection for pancreatic glycoprotein zymogens and serum amylase. Thus, AP is associated with the destruction of the glycoprotein zymogens, which is differentially protected by vitamin E and metformin.

DenSFFNet: dense spiking forward fractional network for cardiovascular risk prediction using retinal fundus images in spark framework.

P K, G A, Gouni R

Arch Physiol Biochem · 2025 Oct · PMID 40489256 · Publisher ↗

Cardiovascular risk prediction identifies individuals at high risk before symptoms arise. To address challenges such as integrating diverse data, ensuring quality, and managing patient variability, the Dense Spiking Forw... Cardiovascular risk prediction identifies individuals at high risk before symptoms arise. To address challenges such as integrating diverse data, ensuring quality, and managing patient variability, the Dense Spiking Forward Fractional Network (DenSFFNet) model is introduced within the Spark framework. The process begins with image acquisition and partitioning using Deep Embedded Clustering (DEC), followed by preprocessing tasks like Greyscale Conversion, Optic Disc (OD) segmentation with Channel Prior Convolutional Attention (CPCA), and blood vessel segmentation using Frangi-Net across slave nodes. Extracted features, including Learned Invariant Feature Transformation (LIFT) and statistical metrics, are aggregated by the master node, which utilises the DenSFFNet model a combination of DenseNet and Deep Spiking Neural Network (DSNN). The DenSFFNet method attained accuracy, sensitivity, specificity, and Matthews correlation coefficient (MCC) is 91.119%, 90.366%, 89.922%, and 92.643% for dataset 1. For the RFMiD 2.0 dataset, the proposed method attained 90.881% accuracy, 90.286% sensitivity, 89.660% specificity, and 91.469% MCC.

Research advance in mesenchymal stem cell-based therapy for diabetic nephropathy.

Hui Y, Dong Y, Liu Y

Arch Physiol Biochem · 2025 Jun · PMID 40482673 · Publisher ↗

Diabetic nephropathy (DN) is the main cause of end-stage kidney disease and has become a global public health problem. Currently, treatment of DN is limited to alleviating disease progression rather than curing diseases... Diabetic nephropathy (DN) is the main cause of end-stage kidney disease and has become a global public health problem. Currently, treatment of DN is limited to alleviating disease progression rather than curing diseases or restoring renal function, thus more effective therapeutic strategies against DN are urgently needed. Mesenchymal stem cells (MSCs) have been widely applied in the prevention and treatment of DN. Preclinical studies have proved that MSCs exhibited favourable therapeutic effects on DN by regulation of hyperglycaemia, reduction of urinary albumin, and protecting renal function. Hence this review provides an overview of the biological properties of MSCs, summarises the regulatory mechanisms of MSC-based therapy for DN, presents ongoing or completed clinical trials, as well as discusses the potential challenges and new strategies of MSCs in the treatment of DN, with the aim of providing a balanced and unbiased view of MSC transplantation as promising therapeutic strategies for DN.

Living high-training low model promotes increased spontaneous physical activity, reduced adiposity and maintenance of fat-free mass in C57BL/6J mice.

Orsi JB, Scariot PPM, Polisel EEC … +5 more , Araujo LS, Santos MR, Papoti M, Manchado-Gobatto FB, Gobatto CA

Arch Physiol Biochem · 2025 Dec · PMID 40476650 · Publisher ↗

Researchers have extensively studied how hypoxia affects physiological variables, with training models like "live high - train low" (LH-TL) proposed by Levine & Stray-Gundersen in 1997 to improve athletic performance. Al... Researchers have extensively studied how hypoxia affects physiological variables, with training models like "live high - train low" (LH-TL) proposed by Levine & Stray-Gundersen in 1997 to improve athletic performance. Although well-known, few studies use animal models for more in-depth analyses than human studies allow. This study investigated the effects of aerobic training on adiposity, spontaneous physical activity (SPA), and food and water intake in C57BL/6J mice housed in normoxic (Nx) or hypoxic (Hx) conditions for 8 weeks. Mice were divided into trained (T) and sedentary (S) groups, with 10 mice each. Hx animals were kept in normobaric hypoxia (FiO=14.5%) for 18 h/day. Training was done at 80% critical velocity, 5 times/week in normoxia. The T groups had lower SPA, especially the Hx-T group, which showed higher food and water intake, reduced fat, and a higher fat-free mass/carcass fat mass ratio. Findings suggest exercise and hypoxia may help combat obesity.

Statement of Retraction: Comparison and performance evaluation of human bio-field visualization algorithm.

Arch Physiol Biochem · 2025 Dec · PMID 40449015 · Publisher ↗

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Pharmacotherapeutic potentials of astragalin against cisplatin-induced renal toxicity via regulating Nrf-2/keap-1 pathway.

Ijaz MU, Furqan R, Salar MZ … +3 more , Hamza A, Ashraf A, Hamdi H

Arch Physiol Biochem · 2025 Dec · PMID 40418170 · Publisher ↗

PURPOSE: Cisplatin (CP) is a chemotherapeutic drug that can produce toxic effects in many organs of the body including kidney. Thus, the current trial was executed for 30 days to assess the alleviative effects of AST to... PURPOSE: Cisplatin (CP) is a chemotherapeutic drug that can produce toxic effects in many organs of the body including kidney. Thus, the current trial was executed for 30 days to assess the alleviative effects of AST to avert CP instigated renal injuries. MATERIALS AND METHODS: Forty-eight male albino rats were allocated into four groups including control, CP (10 mg/kg), CP+AST (10 mg/kg + 50mg/kg) and only AST (50 mg/kg). On the completion of trial, the rats were dissected and further analyses were performed. RESULTS: CP intoxication increased the expressions of pro-apoptotic markers (Caspase-3 and Bax) while reducing the expressions of Nrf-2 and antiapoptotic marker (Bcl-2) and lowering the expressions and activities of antioxidant enzymes i.e., GPx, GSR, CAT, HO-1, GST, SOD and GSH contents. Furthermore, CP intoxication elevated the levels of oxidative stress markers (MDA and ROS) and inflammatory markers (IL-6, IL-1 β, TNF-α, NF-kB and COX-2). CP exposure also disrupted the levels of renal function markers and renal histology. However, AST treatment ameliorated all the renal alterations induced by CP-exposure. CONCLUSION: Therefore, AST protected the renal tissues from CP-instigated damages due to its antioxidant and reno-protective potential.

The role of coenzyme Q10 in exercise tolerance and muscle strength.

Bian Z, Wei L

Arch Physiol Biochem · 2025 Dec · PMID 40411469 · Publisher ↗

: 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) an... : 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). : This review will explore the mechanisms of CoQ10, its impact on exercise performance to be addressed. : 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.

Evaluation of leptin and leptin receptor gene polymorphisms in bipolar disorder: focus on depressive episodes with atypical features.

Aytac HM, Oyaci Y, Aytac E … +3 more , Pehlivan M, Alptekin FB, Pehlivan S

Arch Physiol Biochem · 2025 Dec · PMID 40407704 · Publisher ↗

: Our study aims to examine the effect of leptin () (-2548 G > A) (rs7799039) and leptin receptor () (668 A > G) (rs1137101) gene polymorphisms on the etiopathogenesis of bipolar disorder (BD) by comparing them with a co... : Our study aims to examine the effect of leptin () (-2548 G > A) (rs7799039) and leptin receptor () (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. : 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). : The distribution of genotypes was significantly different between BD patients and healthy controls. Specifically, the homozygous 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 AA and GG genotypes were significantly more common among patients with a history of atypical depression. Logistic regression showed that the polymorphism and Hamilton Depression Rating Scale (HAM-D) score predict atypical depression in BD. : In summary, while the polymorphism is linked to BD, the polymorphism and symptom severity appear to predict atypical depressive episodes.

The antioxidant and anti-inflammatory effects of gallic acid and/or cerium oxide nanoparticles synthesized by gamma-irradiation ameliorate cisplatin-induced hepatic injury.

Saif-Elnasr M, Elmalawany AM, Abdel-Khalek AF

Arch Physiol Biochem · 2025 Dec · PMID 40402839 · Publisher ↗

CONTEXT: Cisplatin is a widely utilised chemotherapeutic agent for cancer therapy, but various systemic toxicities limit its effectiveness. OBJECTIVE: This study aimed to assess the hepatoprotective properties expressed... CONTEXT: Cisplatin is a widely utilised chemotherapeutic agent for cancer therapy, but various systemic toxicities limit its effectiveness. OBJECTIVE: 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. MATERIALS AND METHODS: 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. RESULTS: 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. DISCUSSION AND CONCLUSION: 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.

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.

Zobeydi AM, Kordi MR, Gharakhanlou R … +2 more , Khalounejad H, Parastesh M

Arch Physiol Biochem · 2025 Oct · PMID 40397783 · Publisher ↗

AIMS: 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... AIMS: 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. MAIN METHODS: 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. KEY FINDINGS: 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. SIGNIFICANCE: 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.

The impact of a multi-species probiotic supplementation on clinical symptoms and biochemical factors in patients with irritable bowel syndrome: a randomised controlled trial.

Hajiani S, Tajabadi Ebrahimi M, Sadeghi A … +2 more , Zarrabi Ahrabi N, Yadegar A

Arch Physiol Biochem · 2025 Dec · PMID 40392916 · Publisher ↗

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 qualit... 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. 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. 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. This multi-species probiotic supplement was safe and effective in reducing symptom severity and improved QOL of IBS patients.

Heptaminol-induced metabolic liver and cardiac injuries in rats: phytochemical screening, experimental, computational modelling and pharmacological study of seeds.

Abbassi R, Bouzenna H, Badraoui R … +9 more , Atwan M, Brahmi F, Feriani A, Siddiqui AJ, Adnan M, Mohajja A, Choura S, Chamkha M, Hfaiedh N

Arch Physiol Biochem · 2025 Oct · PMID 40372243 · Publisher ↗

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... 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 (DSPE) by GC-MS analysis and to assess the antioxidant, anticoagulant and ACE activities. The hepato and cardiotoprotective effect against HEP-induced toxicity in rats have been assessed using biochemical, histological and computational assays. 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. 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.

Comparable hepatocellular metabolomic signatures under glucose and palmitic acid treatment relative to butyrate in relation to metabolic dysfunction-associated fatty liver disease.

Nehal, Jyoti, Dey P

Arch Physiol Biochem · 2025 Oct · PMID 40372011 · Publisher ↗

INTRODUCTION: Among the dietary factors, glucose, and fatty acids are known to trigger fatty liver disease, while butyrate attenuates steatosis. OBJECTIVE: To decipher the hepatocellular altered metabolome under nutrient... INTRODUCTION: Among the dietary factors, glucose, and fatty acids are known to trigger fatty liver disease, while butyrate attenuates steatosis. OBJECTIVE: To decipher the hepatocellular altered metabolome under nutrient perturbation relevant to fatty liver disease. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Selenium deficiency modulates neonatal pulmonary alveolar development via mitochondrial ROS accumulation and oxidative stress mediated by STAT3 inhibition.

Tan HY, Xiang YL, Tan MJ … +3 more , Fang CC, Zhang YP, Peng F

Arch Physiol Biochem · 2025 Oct · PMID 40367139 · Publisher ↗

: Recent findings suggest that Selenium (Se) deficiency in neonates may hinder pulmonary alveolar development, but the underlying molecular mechanisms remain underexplored. : This study utilised a neonatal mouse model to... : Recent findings suggest that Selenium (Se) deficiency in neonates may hinder pulmonary alveolar development, but the underlying molecular mechanisms remain underexplored. : This study utilised a neonatal mouse model to investigate the effects of dietary Se deficiency on pulmonary alveolar development. : 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. : 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. : 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.

Evaluation of for hepatoprotection, hematological assessment and inhibitor of TGFβR1 in liver diseases.

Ololade ZS, Anuoluwa IA, Onifade OF … +4 more , Adeagbo AI, Oyebanji OT, Asaju AO, Eze JC

Arch Physiol Biochem · 2025 Oct · PMID 40364510 · Publisher ↗

BACKGROUND: This study was conducted to assess the hepatoprotective potential of Annona muricata flower (AMF) using albino rats' model. MATERIALS AND METHODS: Liver function assays such as alkaline phosphatase (ALP), ala... BACKGROUND: This study was conducted to assess the hepatoprotective potential of Annona muricata flower (AMF) using albino rats' model. MATERIALS AND METHODS: 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. RESULTS AND DISCUSSION: 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. CONCLUSION: This study provides information on the uses of AMF as a natural product for hepatoprotection and other therapeutic purposes.

Cholecalciferol alleviates testicular dysfunction in experimental hyperthyroidism via antioxidant, anti-inflammatory and antiapoptotic effects.

Salem HR, Kasem HA

Arch Physiol Biochem · 2025 Oct · PMID 40359124 · Publisher ↗

BACKGROUND: This study aimed to investigate the possible protective effect of cholecalciferol against testicular dysfunction in L-thyroxine-induced hyperthyroid rat model. METHODS: Twenty-four adult male rats were divide... BACKGROUND: This study aimed to investigate the possible protective effect of cholecalciferol against testicular dysfunction in L-thyroxine-induced hyperthyroid rat model. METHODS: 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. RESULTS: 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. CONCLUSION: Cholecalciferol could ameliorate pathophysiological changes in rat testes of hyperthyroid rats.
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