Archives of Physiology and Biochemistry最新文献

Context: 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).

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

Results: 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.

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 (FiO₂=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.

Background: Verbascoside (VB) inhibits endoplasmic reticulum stress (ERS), but its therapeutic potential in hypertension (HTN) is unclear.

Aim: To investigate whether VB inhibits ERS by modulating the Nur77/GFPT2/CHOP axis, thereby ameliorating angiotensin II (Ang II)-induced HTN.

Methods: The cell biological behaviour of HUVECs was determined by CCK-8, LDH kit, scratch assay, and adhesion assay. Oxidative stress factor levels were detected by flow cytometry and kits. The levels of ERS and the Nur77/GFPT2/CHOP pathway-related proteins were examined through Western blot.

Results: VB increased the viability of Ang II-treated HUVECs, inhibited LDH release, and reduced cell migration and adhesion. VB also reduced ERS marker protein levels, while inhibiting oxidative stress and modulating the Nur77/GFPT2/CHOP pathway. VB lowered blood pressure and increased elastic fibre deposition in HTN mice, and Nur77 agonists enhanced the protective impact of VB.

Conclusion: VB hindered Ang II-induced endothelial dysfunction and ERS through modulating the Nur77/GFPT2/CHOP pathway.

As people pay more and more attention to health management and exercise, the demand for monitoring fat metabolism and sports injuries is increasing day by day. Fat metabolism, as an important component of human energy metabolism, is closely related to athletic performance, weight management and the prevention of chronic diseases. Through high-precision optical sensors and advanced data analysis algorithms, this method can capture the changes in human physiological signals in real time, thereby reflecting the state of fat metabolism and the occurrence of sports injuries. This research provides new ideas and methods for fat metabolism monitoring and sports injury prevention and is expected to be widely applied in fields such as sports health management, sports training guidance. Through this real-time monitoring technology, people can better understand their own fat metabolism, formulate scientific exercise and diet plans, effectively prevent and promptly handle sports injuries, and improve exercise effectiveness and health levels.

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that induces significant oxidative damage to the male reproductive system. This study evaluates the protective effects of gut-derived Indolepropionic acid (IPA) against testicular damage in streptozotocin (STZ) induced T2DM rats. T2DM was induced in male rats with a high-fat diet and STZ (50 mg/kg). Groups included: Control, T2DM, T2DM + IPA, IPA only, and T2DM + Metformin, treated for four weeks. T2DM + IPA showed a significantly improved gonadosomatic index, healthier seminiferous tubules histology, characterised by the presence of spermatogonia and elongated spermatozoa and more viable sperm. T2DM + IPA also revealed reduced oxidative stress (elevated superoxide dismutase and catalase, lower malondialdehyde) and upregulated KISS1 and LDH-C gene expressions while downregulated FGF21, compared to T2DM and T2DM + Metformin groups. These findings suggest IPA protects against diabetic testicular toxicity by enhancing antioxidant defences and modulating key metabolic and spermatogenic genes.

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.

Chronic sinusitis with nasal polyps (CRSwNP) has a relatively high recurrence rate, seriously affecting the quality of life of patients. Neuroinflammation interacts with the persistent inflammatory state of the nasal mucosa. This study aims to explore the application value of medical thermal imaging technology in predicting postoperative recurrence of nECRSwNP, and to evaluate potential biomarkers and efficacy assessment methods for neuroinflammation treatment, with the expectation of providing new strategies for reducing postoperative recurrence rates and improving the quality of life. Medical thermal imaging technology can monitor the temperature changes of nasal mucosa in real time and promptly detect alterations in inflammatory activity. The levels of EOS and cytokines in peripheral blood can serve as potential biomarkers for evaluating the status of neuroinflammation, which is helpful for identifying patients with a higher risk of recurrence, thereby enabling timely adjustment of treatment plans and improving the pertinence and effectiveness of neuroinflammation treatment.

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.

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.