Archives of Physiology and Biochemistry最新文献

Introduction: Orthopaedic repair outcomes are limited by disrupted cellular mechanotransduction and physiological instability during anaesthesia. Integrating biomechanical signal modulation with stabilising perioperative strategies may enhance tissue healing and reduce postsurgical complications. Methodology: Existing orthopaedic therapies fail to restore native mechanosensory signalling at repair sites, leading to delayed recovery, implant loosening, and reduced function. Additionally, anaesthesia-induced cardiovascular and metabolic changes disrupt regenerative signalling. This paper presents GEM-TRAP, a synergistic cotargeting platform using dual delivery of gene vectors to enhance mechanotransduction and protein regulators to maintain physiological stability during anaesthesia. Smart biomaterial scaffolds enable controlled release at the injury site. Results: In vivo results show improved osseointegration, a 38% increase in load-bearing strength, enhanced neural-mechanical signalling, and a 27% reduction in complications, demonstrating GEM-TRAP's potential for advanced orthopaedic regeneration. The proposed method achieves the osseointegration efficiency of 90%, physiological stability of 92%, mechanical strength recovery of 90%, mitochondrial efficiency of 90%, and postsurgical complications reduced by 40-60%. Conclusion: This study presents GEM-TRAP, a novel cotargeting platform that concurrently enhances cellular mechanotransduction and maintains physiological stability during anaesthesia. By integrating dual therapeutic delivery with smart biomaterial scaffolds, the approach addresses both regenerative and perioperative challenges, offering a new strategy for improving orthopaedic repair and functional recovery.

Context: Sirtuin-2 (SIRT2) is a longevity-related protein implicated in apoptosis, metabolic regulation and oxidative stress; however, its role in ageing pancreas remains unclear. Objective: This study investigated the effects of the selective SIRT2 inhibitor, Arabidopsis guanylate kinases-2 (AGK-2) on oxidative stress and apoptosis in aged rat pancreatic tissue. Methods: Young (3-month) and aged (22-month) Wistar albino rats were divided into control and AGK-2-treated groups (10 μM, 30 days). Total oxidant status (TOS) and total antioxidant status (TAS) used commercial kits, then calculated Oxidative stress index (OSI). For detecting nitrosative stress, we determined nitrite-nitrate levels using the Griess test. SIRT2 and caspase-3 were evaluated by ELISA and Western blot. Discussion and conclussion: Our findings showed that ageing increased SIRT2 expression, oxidative stress and caspase-3 protein compared to young rats. AGK-2 treatment reduced SIRT2, TOS, OSI and caspase-3, and increased TAS particularly in aged rats. AGK-2 reverses ageing-associated changes in pancreatic oxidative stress and apoptosis. SIRT2 modulation may represent a potential therapeutic target against age-related pancreatic degeneration.

Kidney injury is a common complication of obesity. This study evaluated the protective effect of the prebiotic fructooligosaccharide (FOS) on kidney injury in a high-fat diet-induced obese rat model. Obese rats exhibited increased body weights, elevated lipid profiles, decreased plasma lipopolysaccharide-binding protein (LBP), elevated kidney malondialdehyde (MDA), increased superoxide dismutase (SOD) activity, and histopathological damage. They also show reduced nephrin expression and upregulated mRNA levels of kidney injury molecule-1 (KIM-1) and renin. Supplementation with 10% FOS significantly reduced body weight and triglyceride levels, restored plasma LBP, decreased kidney MDA levels, and enhanced SOD activity. FOS also prevented the upregulation of KIM-1 and renin mRNA and restored nephrin expression. These findings suggest that FOS mitigates obesity-induced kidney injury, supporting its potential as a preventive nutritional intervention.

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.

Objective: 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.

Materials and methods: 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.

Results and discussion: 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 K_i values of GSH and ascorbic acid were calculated as 0.48 µM and 30.47 µM, respectively.

Conclusion: 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.

Post-thrombotic syndrome (PTS), a chronic complication of deep vein thrombosis, causes pain, swelling, and ulcers, impairing quality of life. This study explores the role of lipid peroxidation and chronic inflammation in PTS. Oxidative stress and chronic inflammation damage the endothelium, increase venous pressure, and induce fibrosis, driving PTS progression. A biomarker-based ELISA approach is proposed to measure plasma lipid peroxidation products (e.g. MDA) and pro-inflammatory cytokines (e.g. IL-6, TNF-α). This method detects early biochemical changes in post-DVT patients and tracks PTS risk. Elevated oxidative and inflammatory markers are strongly linked to PTS, supporting their use as diagnostic and therapeutic targets. Screening may improve prediction (98.7%), prevention (97.3%), and management (99.4%), while reducing MDA (95.6%), IL-6 (93.4%), and TNF-α (97.45%). Observational NHS data support symptom-biomarker correlations. Preliminary values for MDA (14.3 ± 4.1 nmol/mL), IL-6 (2.3 ± 1.1 pg/mL), and TNF-α (1.5 ± 0.7 pg/mL) are included to clearly present and support the research hypothesis.

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.

Background: Metabolic syndrome (MetS) involves insulin resistance and dyslipidemia.

Objective: To evaluate vitamin D's (Vit D) hepatoprotective role in MetS and its mechanisms.

Methods: Thirty male rats were divided into MetS, MetS + Vit D, and control groups. We measured arterial blood pressure (ABP), body weight, fat, homeostatic Model Assessment for Insulin Resistance (HOMA-IR), glycemic/lipid profiles, liver enzymes, oxidative stress (Malondialdehyde, superoxide dismutase), inflammation (Tumor necrosis factor; TNF-α, matrix metalloproteinase; MMP9, Glial fibrillary acidic protein; GFAP), and AMP-activated protein kinase/Phosphoinositide 3-kinase (AMPK/PI3K) expression.

Results: MetS increased oxidative stress, TNF-α, liver enzymes, HOMA-IR, and ABP while reducing adiponectin and AMPK/PI3K. Vit D reversed these effects, suppressing GFAP/MMP9 and restoring metabolic balance. Conclusion: Vit D mitigates MetS-induced liver damage via AMPK/PI3K activation, exerting antioxidant and anti-inflammatory effects.

Objective: This study aimed to investigate the effects of circ-RPL15 on epithelial mesenchymal transformation (EMT) and tumour growth in non-small cell lung cancer (NSCLC).

Methods: circ-RPL15, microRNA (miR)-518c-3p and WD repeat protein 1 (WDR1) in tumour tissues were detected. Cell viability, apoptosis, migration and invasion, and EMT were analysed in A549 cells after altering circ-RPL15 or miR-518c-3p expression. The targeting relationship between miR-518c-3p with circ-RPL15 or WDR1 was verified.

Results: The results elucidated that circ-RPL15 and WDR1 levels were elevated in NSCLC tissues, while miR-518c-3p was downregulated. Suppressing circ-RPL15 or elevating miR-518c-3p suppressed cell growth and delayed EMT process. miR-518c-3p was found to target both circ-RPL15 and WDR1, and increasing WDR1 counteracted the effects of reducing circ-RPL15 on A549 cells. Downregulating circ-RPL15 suppressed tumour growth in NSCLC in vivo.

Conclusion: Shortly, circ-RPL15 accelerates EMT and tumour growth in NSCLC via modulating the miR-518c-3p/WDR1 axis.