Archives of Physiology and Biochemistry最新文献

Objective: This study investigated the clinical significance of serum miR-339-5p in MASLD and explored its molecular mechanisms in hepatic steatosis and inflammation.

Methods: 87 MASLD patients (Np-MASLD, n = 51; MASH-F, n = 36) were enrolled. Serum miR-339-5p was quantified and correlated with clinical indices. In vitro studies used FFA-treated HepG2 cells to assess miR-339-5p and SORT1 effects on lipid accumulation, inflammation.

Results: Serum miR-339-5p was significantly elevated in MASLD, correlating positively with disease severity, and served as an independent risk factor for MASH-F progression. In HepG2 cells, miR-339-5p overexpression exacerbated FFA-induced lipid accumulation and IL-6/TNF-α secretion, whereas its inhibition exerted protective effects. SORT1 was validated as a direct target of miR-339-5p and was downregulated in MASLD. miR-339-5p suppressed AMPK phosphorylation and promoted NF-κB activation by targeting SORT1.

Conclusion: Elevated miR-339-5p promotes hepatocyte lipid accumulation and inflammation in MASLD, potentially by targeting SORT1.

Background: Long non-coding RNAs (lncRNAs) play pivotal roles in diverse diseases, including non-alcoholic fatty liver disease (NAFLD). This study aimed to explore the expression of LINC00240 in NAFLD patients, elucidating its potential as a biomarker.

Methods: RT-qPCR was employed to measure the levels of LINC00240 and miR-133a-3p. ROC curve analysed diagnostic value, luciferase reporter assay verified their targeting relationship, and lipid metabolism markers were detected for correlation analysis.

Results: Serum LINC00240 was upregulated and miR-133a-3p was downregulated in NAFLD patients. LINC00240 was positively correlated with TC, TG, ALT, and HOMA-IR. Both LINC00240 and miR-133a-3p displayed diagnostic potential. LINC00240 directly targeted miR-133a-3p. Knockdown of LINC00240 reduced lipid metabolism parameters, while was partially reversed by miR-133a-3p antagomir.

Conclusion: LINC00240 and miR-133a-3p are potential diagnostic biomarkers for NAFLD. LINC00240/miR-133a-3p axis modulates NAFLD progression by regulating hepatic steatosis and insulin resistance, suggesting an antagonistic regulatory mechanism underlying NAFLD progression and lipid metabolic dysregulation.

Background: With rapid global population ageing, older women bear a disproportionate burden of cognitive impairment, depression, and anxiety. Reproductive history, a unique and irreversible life course factor, may influence late-life cognitive and mental health.

Methods: We included 4,173 women aged ≥65 years from the 2017-2018 China Longitudinal Healthy Longevity Survey. Standard scales assessed cognition and mood, followed by regression, network, and two-sample MR analyses.

Results: After adjustment, having more than four births was associated with a lower risk of cognitive impairment (OR = 0.66, 95% CI: 0.48-0.91). Network analysis identified restlessness and uncontrollable worry as central symptoms, with language and attention as key bridge nodes. MR analyses linked higher parity to poorer cognition and later first birth to better cognition and lower depression risk.

Conclusion: Reproductive history is linked to late-life cognitive and emotional health through sociocultural and biological mechanisms, highlighting the importance of population-specific precision health strategies.

Context: Health plays an essential role in human life, particularly brain health, which supports vital system functions. Magnetic Resonance Imaging (MRI) is a crucial tool for diagnosing brain-related disorders and provides large datasets suitable for artificial intelligence, especially image classification. Objective: The aim of this study is to develop an accurate and reliable deep learning-based framework for the automatic classification of brain tumours (glioma, meningioma, and pituitary tumours) from MRI images. Materials and methods: Pre-processing is performed using the Adaptive Contrast Enhancement Algorithm (ACEA) and a median filter. For segmentation, Weighted Fuzzy C-means clustering (WFCMC) ensures reliable pixel assessment, normalisation, and generalisation. Image regularisation is achieved by scaling and analysing data loss to maintain pixel stability. A novel Ensembling Dense Convolutional Neural Network with Bayesian Auto-encoder (E-DCNNBAE) model is proposed for classification. Results: The performance of model is evaluated using accuracy, precision, recall, F-score, and AUC. It achieves 97% accuracy, 99% precision, 98% recall, 98% F-score, and 98% AUC. Conclusion: This study improving early diagnosis and treatment of brain diseases.

Context: Diabetic kidney disease (DKD) presents substantial challenges in early detection and clinical monitoring. Mitochondrial dysfunction plays a pivotal role in DKD pathogenesis, and mitochondrial DNA copy number (mtDNA-CN) reflects this dysfunction. Objective: To evaluate the translational potential of mtDNA-CN as a biomarker for DKD, focusing on its diagnostic, prognostic, and monitoring utility across biological specimens, and examine the critical challenges of its clinical translation. Materials and Methods: We systematically synthesize evidence from cellular experiments, animal models, and clinical studies that assess mtDNA-CN alterations in DKD, with a comparative analysis of specimen types and methodologies. Results: Studies demonstrated that mtDNA-CN in blood and urine are correlated with the onset and progression of DKD. Rigorous standardization must be implemented across specimen collection, pre-analytical processing, analytical testing, detection and data reporting. Conclusion: MtDNA-CN is a promising and measurable biomarker for DKD. Combined with conventional markers, it could enhance clinical utility.

Background: Globally, preterm birth continues to be a major contributor to neonatal morbidity and mortality. Developing early diagnostics and focused interventions requires an understanding of the molecular and microbiome factors causing preterm birth and also the identification of biomarkers. Methods: We integrated gut microbiome and DNA methylation data to identify biomarkers of preterm birth. Analysis of GSE120458 revealed 1,609 differentially methylated regions involved in immune, hormonal, and neurodevelopmental pathways. Microbiome profiling identified five altered genera: Faecalibacterium prausnitzii, Streptococcus, Blautia faecis, Gemella, and Agathobacter. Taxon Set Enrichment Analysis revealed that these genera were found to be associated with systemic diseases like diabetes, obesity, and inflammatory bowel disease. Results: We identified 1,649 genes targeted by 33 microbial metabolites, with 17 overlapping methylated genes indicating microbiome-epigenome interactions. These genes were linked to neuroimmune and synaptic pathways. Conclusion: Hub genes may serve as biomarkers for early intervention. Overall, the results connect microbial metabolism with epigenetic regulation in preterm birth.

Background: Acute Respiratory Distress Syndrome (ARDS) is a life-threatening condition associated with high morbidity and mortality, characterized by severe inflammation, oxidative stress, impaired gas exchange, and progressive lung injury. Disruption of cellular redox homeostasis plays a central role in ARDS pathogenesis, making redox-regulatory mechanisms attractive therapeutic targets. Methods: This review evaluates experimental evidence on protein-mediated regulation of oxidative stress pathways in ARDS, focusing on proteins involved in antioxidant defense, reactive oxygen species (ROS) generation, mitochondrial signaling, and maintenance of cellular redox homeostasis. Results: Current evidence indicates that key regulatory proteins modulate oxidative stress by activating endogenous antioxidant defense systems, regulating ROS production, and influencing mitochondrial signaling pathways. These mechanisms reduce oxidative damage and pulmonary inflammation while preserving cellular redox balance. Experimental studies further demonstrate that modulation of specific protein regulators enhances cellular resilience under hypoxic and inflammatory conditions characteristic of ARDS. Conclusions: Protein-mediated regulation of redox signaling represents a promising therapeutic strategy for ARDS. Targeting redox-regulatory proteins may attenuate oxidative stress, reduce lung inflammation, and improve cellular survival, supporting their potential as novel therapeutic targets. Further preclinical and clinical studies are needed to validate these findings and facilitate their translation into clinical practice.

Diabetes mellitus is associated with neurochemical and lung imbalances. This study investigates the therapeutic potential of exosome (Exo) treatment in ameliorating systemic complications in a rat model of type 2 diabetes. Eighteen male rats were divided into three groups: Control, Diabetic, and Diabetic + Exosome-treated. After the intervention period, serum, brain, and lung tissues were analysed. In serum, diabetes induced hyperglycaemia and dyslipidaemia, all of which were significantly improved by Exo (p < 0.001). Diabetic rats exhibited significant elevations in brain malondialdehyde, mTOR, and GSK3β, along with reduced glutathione, serotonin, and dopamine (all p < 0.001 vs. Control). Exo treatment reversed these changes (p < 0.001 vs. Diabetic). In lung tissue, diabetes increased MDA, TRPM2, and NLRP3 while suppressed superoxide dismutase; Exo treatment ameliorated these issues (p < 0.001). Exosomes exert potent antioxidant and anti-inflammatory in type 2 diabetic rats in the brain and lungs.

Background: This multicentre study examined the association between TCM syndromes and HRM parameters in GERD patients. Methods: GERD patients were classified into seven syndromes and assessed for LESP, LESL, IRP, DL, DCI, IEM, and fragmented peristalsis. Results: HRM parameters differed significantly among TCM syndromes (p < 0.01). Liver-Stomach Depression Heat (28.3%, 128/452) and Gallbladder Heat Attacking Stomach (12.4%, 56/452) showed higher LESP (18.5 ± 4.2 and 17.8 ± 3.9 mmHg) and DCI, indicating hypermotility. Middle Deficiency with Qi Counterflow (18.1%, 82/452) and Stomach Yin Deficiency (9.3%, 42/452) showed lower LESP (9.2 ± 2.8 and 8.5 ± 2.5 mmHg) and higher IEM (68.3% and 73.8%), indicating hypomotility. Qi Depression and Phlegm Obstruction (15.0%, 68/452) correlated with fragmented peristalsis (35.3%). Blood Stasis Obstructing the Collaterals (5.8%, 26/452) showed increased IRP (11.2 ± 3.5 mmHg) and abnormal coordination, and Spleen Deficiency with Dampness-Heat was mainly hypomotile. Conclusion: TCM syndromes in GERD correspond to distinct HRM patterns.

Background: The prevalence of exercise metabolic syndrome (MetS) has prompted research on effective intervention strategies, particularly high-intensity interval training (HIIT) and its potential in combination with exercise nutrition.

Purpose: The study aims to explore the specific molecular mechanism of AMPK phosphorylation regulation in improving exercise metabolic syndrome in HIIT.

Method: By detecting the structural characteristics and phosphorylation status of AMPK, analyse its regulatory effect on metabolism.

Results: The results showed that HIIT significantly promoted the phosphorylation of AMPK and enhanced its regulatory ability on energy metabolism. Meanwhile, the expression of MG53 protein was upregulated with the implementation of HIIT and exercise nutrition, indicating its critical role in muscle cell repair and metabolic regulation.

Conclusion: Therefore, the phosphorylation regulation of AMPK plays a central role in the improvement of exercise metabolic syndrome by HIIT, and MG53 protein, as an important regulatory factor, may enhance the effectiveness of HIIT by promoting cell repair and metabolic regulation.