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Major depressive disorder is a serious mental disorder with high morbidity and mortality. The role of social stress in the development of depression remains unclear. Here, we used the social defeat stress paradigm to induce depression-like behavior in rats, then evaluated the behavior of the rats and measured metabolic changes in the prefrontal cortex using gas chromatography-mass spectrometry. Within the first week after the social defeat procedure, the sucrose preference test (SPT), open field test (OFT), elevated plus maze (EPM) and forced swim test (FST) were conducted to examine the depressive-like and anxiety-like behaviors. For our metabolite analysis, multivariate statistics were applied to observe the distribution of all samples and to differentiate the socially defeated group from the control group. Ingenuity pathway analysis was used to find the potential relationships among the differential metabolites. In the OFT and EPM, there were no significant differences between the two experimental groups. In the SPT and FST, socially defeated rats showed less sucrose intake and longer immobility time compared with control rats. Metabolic profiling identified 25 significant variables with good predictability. Ingenuity pathways analysis revealed that \"Hereditary Disorder, Neurological Disease, Lipid Metabolism\" was the most significantly altered network. Stress-induced alterations of low molecular weight metabolites were observed in the prefrontal cortex of rats. Particularly, lipid metabolism, amino acid metabolism, and energy metabolism were significantly perturbed. The results of this study suggest that repeated social defeat can lead to metabolic changes and depression-like behavior in rats.

Background Sex and reproductive status differences exist in both non-alcoholic fatty liver disease (NAFLD) and body composition. Our purpose was to investigate the relationship between body composition and the severity of liver steatosis and fibrosis in NAFLD in different sex and reproductive status populations. Methods This cross-sectional study included 880 patients (355 men, 417 pre-menopausal women, 108 post-menopausal women). Liver steatosis and fibrosis and body composition data were measured using FibroScan and a bioelectrical impedance body composition analyzer (BIA), respectively, and the following parameters were obtained: liver stiffness measurement (LSM), controlled attenuation parameter (CAP), waist circumference (WC), body mass index (BMI), percent body fat (PBF), visceral fat area (VFA), appendicular skeletal muscle mass (ASM), appendicular skeletal muscle mass index (ASMI), fat mass (FM), fat free mass (FFM), and FFM to FM ratio (FFM/FM). Multiple ordinal logistic regression (MOLR) was used to analyze the independent correlation between body composition indicators and liver steatosis grade and fibrosis stage in different sex and menopausal status populations. Results Men had higher WC, ASM, ASMI, FFM, and FFM/FM than pre- or post-menopausal women, while pre-menopausal women had higher PBF, VFA, and FM than the other two groups (p < 0.001). Besides, men had greater CAP and LSM values (p < 0.001). For MOLR, after adjusting for confounding factors, WC (OR, 1.07; 95% CI, 1.02–1.12; P = 0.011) and FFM/FM (OR, 0.52; 95% CI, 0.31–0.89; P = 0.017) in men and visceral obesity (OR, 4.16; 95% CI, 1.09–15.90; P = 0.037) in post-menopausal women were independently associated with liver steatosis grade. WC and visceral obesity were independently associated with liver fibrosis stage in men (OR, 1.05; 95% CI, 1.01–1.09, P = 0.013; OR, 3.92; 95% CI, 1.97–7.81; P < 0.001, respectively). Conclusions Increased WC and low FFM/FM in men and visceral obesity in post-menopausal women were independent correlates of more severe liver steatosis. In addition, increased WC and visceral obesity were independent correlates of worse liver fibrosis in men. These data support the sex- and reproductive status-specific management of NAFLD.

Our study investigated the role of nicotinamide adenine dinucleotide phosphate (NADPH) in neuroinflammation-associated depression-like behaviors. Using a lipopolysaccharide (LPS)-induced mouse model of depression, we found that NADPH significantly alleviated depressive-like behaviors, including reduced immobility time and increased sucrose preference. Mechanistic exploration revealed that NADPH suppressed microglial activation, downregulated pro-inflammatory cytokine expression (e.g., IL-1β, TNF-α, IFN-γ), and mitigated oxidative stress in the hippocampus, thereby ameliorating neuroinflammation. Furthermore, NADPH preserved myelin integrity, inhibited microglial phagocytosis of myelin and synapses, and preserved synaptic integrity. These findings provide experimental evidence supporting NADPH as a potential antidepressant agent and highlight its critical role in modulating neuroinflammation via dual suppression of cytokine release and microglial hyperactivation.

Depression is a common and disabling mental disorder characterized by high disability and mortality, but its physiopathology remains unclear. In this study, we combined a non-targeted gas chromatography-mass spectrometry (GC-MS)-based metabolomic approach and isobaric tags for relative and absolute quantitation (iTRAQ)-based proteomic analysis to elucidate metabolite and protein alterations in the hippocampus of rat after chronic social defeat stress (CSDS), an extensively used animal model of depression. Ingenuity pathway analysis (IPA) was conducted to integrate underlying relationships among differentially expressed metabolites and proteins. Twenty-five significantly different expressed metabolites and 234 differentially expressed proteins were identified between CSDS and control groups. IPA canonical pathways and network analyses revealed that intracellular second messenger/signal transduction cascades were most significantly altered in the hippocampus of CSDS rats, including cyclic adenosine monophosphate (cAMP), phosphoinositol, tyrosine kinase, and arachidonic acid systems. These results provide a better understanding of biological mechanisms underlying depression, and may help identify potential targets for novel antidepressants.

Background Depression is a global health concern characterized by high incidence, disability, and disease burden. Neuroimmunity, through the secretion of inflammatory mediators and mediation of neuroinflammation, plays a significant role in depression's pathogenesis. However, the underlying molecular mechanisms remain poorly understood. Methods In this pioneering study, we employed a comprehensive multi‐omics approach, integrating 2‐DE proteomics, liquid chromatography mass spectrometry‐based metabolomics, and real‐time polymerase chain reaction (PCR) array, to investigate the hippocampal molecular profiles of lipopolysaccharide (LPS)‐induced immune inflammation‐related depression. This innovative approach aimed to explore the potential pathogenesis of depression by systematically integrating data across multiple molecular layers. Results Compared to the control group, we identified 81 differential proteins, 44 differential metabolites, and 4 differential mRNAs in LPS‐treated mice. Integrated analysis of these multidimensional data revealed that purine metabolism and glutamate metabolism are the most significantly altered molecular pathways in LPS‐induced depression. Additionally, we constructed the corresponding compound‐reaction‐enzyme‐gene regulatory network. Conclusion This study suggests that purine metabolism and glutamate metabolism may be the underlying mechanisms by which neuroinflammation regulates depression‐like behaviors. Our findings confirm the important role of immune inflammation in depression and provide a new clue for the diagnosis and treatment of this disorder. Notably, the multi‐omics approach employed in this study represents a pioneering effort in the field, providing unprecedented insights into the molecular mechanisms underlying depression. The study focused on a mouse model of depression induced by lipopolysaccharides (LPS) and employed innovative multi‐omics approaches, including two‐dimensional gel electrophoresis (2‐DE) for proteomics, liquid chromatography–mass spectrometry (LC–MS) for metabolomics, and real‐time polymerase chain reaction (PCR) microarray technology to analyze the hippocampus of mice. Through these techniques, we found that compared to the control group, there were 81 differentially expressed proteins, 44 differential metabolites, and 4 differential mRNAs in the mice treated with LPS. The integrated analysis of this multidimensional data revealed that purine metabolism and glutamate metabolism are the most significantly altered molecular pathways in depression induced by LPS.

Major depressive disorder (MDD) is a highly prevalent mental disorder affecting millions of people worldwide. However, a clear causative etiology of MDD remains unknown. In this study, we aimed to identify critical protein alterations in plasma from patients with MDD and integrate our proteomics and previous metabolomics data to reveal significantly perturbed pathways in MDD. An isobaric tag for relative and absolute quantification (iTRAQ)-based quantitative proteomics approach was conducted to compare plasma protein expression between patients with depression and healthy controls (CON). For integrative analysis, Ingenuity Pathway Analysis software was used to analyze proteomics and metabolomics data and identify potential relationships among the differential proteins and metabolites. A total of 74 proteins were significantly changed in patients with depression compared with those in healthy CON. Bioinformatics analysis of differential proteins revealed significant alterations in lipid transport and metabolic function, including apolipoproteins (APOE, APOC4 and APOA5), and the serine protease inhibitor. According to canonical pathway analysis, the top five statistically significant pathways were related to lipid transport, inflammation and immunity. Causal network analysis by integrating differential proteins and metabolites suggested that the disturbance of phospholipid metabolism might promote the inflammation in the central nervous system.

To enhance the inerting effect of nitrogen on large longwall goaf, a novel goaf-inerting method of using a full cross-section nitrogen curtain for a U-shaped ventilation working face is developed. The working principle of the full cross-section nitrogen curtain is elucidated. The design principle and key parameters of the nitrogen curtain needed to achieve an optimum nitrogen injection effect are established. The nitrogen curtain technology is successfully applied to the scenario of fire prevention in the underground goaf. The field study shows that the full cross-section curtain injection of nitrogen exhibits many advantages such as simple operation and homogeneous diffusion. The implementation of the nitrogen curtain reduced the maximum width of the goaf oxidation zone from 70 m to 20 m. And the CO concentration in the upper corner decreased from 21.8 ppm to 11.2 ppm after 18 h of nitrogen injection. After 48 h of injection, the CO concentration in the upper corner remained unchanged and the concentration had reduced to 0 in the lower corner. It was demonstrated that the inerting efficiency of the full cross-section nitrogen curtain reached 86% in the upper corner and 100% in the lower, which is significantly superior to the traditional buried-pipe nitrogen injection method. The effect verifies the effectiveness of the curtain injection method of nitrogen, which can ensure a safe working face production.

Adipose-derived stem cells (ADSCs) and bone marrow-derived stem cells (BMSCs) are considered to be prospective sources of mesenchymal stromal cells (MSCs), that can be used in cell therapy for atherosclerosis. The present study investigated whether ADSCs co-cultured with M1 foam macrophages via treatment with oxidized low-density lipoprotein (ox-LDL) would lead to similar or improved anti-inflammatory effects compared with BMSCs. ADSCs, peripheral blood monocytes, BMSCs and ox-LDL were isolated from ten coronary heart disease (CHD) patients. After three passages, the supernatants of the ADSCs and BMSCs were collected and systematically analysed by liquid chromatography-quadrupole time-of-flight-mass spectrometry (6530; Agilent Technologies, Inc., Santa Clara, CA, USA). Cis-9, trans-11 was deemed to be responsible for the potential differences in the metabolic characteristics of ADSCs and BMSCs. These peripheral blood monocytes were characterized using flow cytometry. Following peripheral blood monocytes differentiation into M1 macrophages, the formation of M1 foam macrophages was achieved through treatment with ox-LDL. Overall, 2×106 ADSCs, BMSCs or BMSCs+cis-9, trans-11 were co-cultured with M1 foam macrophages. Anti-inflammatory capability, phagocytic activity, anti-apoptotic capability and cell viability assays were compared among these groups. It was demonstrated that the accumulation of lipid droplets decreased following ADSCs, BMSCs or BMSCs+cis-9, trans-11 treatment in M1 macrophages derived from foam cells. Consistently, ADSCs exhibited great advantageous anti-inflammatory capabilities, phagocytic activity, anti-apoptotic capability activity and cell viability over BMSCs or BMSCs+cis-9, trans-11. Additionally, BMSCs+cis-9, trans-11 also demonstrated marked improvement in anti-inflammatory capability, phagocytic activity, anti-apoptotic capability activity and cell viability in comparison with BMSCs. The present results indicated that ADSCs would be more appropriate for transplantation to treat atherosclerosis than BMSCs alone or BMSCs+cis-9, trans-11. This may be an important mechanism to regulate macrophage immune function.

This study aims to evaluate the efficacy of the Xietu Hemu prescription (XHP) in improving metabolic dysfunction-associated steatotic liver disease (MASLD) through a Real World Study approach. This was a single-center, prospective, real-world cohort study of 262 patients with MASLD who met the inclusion and exclusion criteria from November 2021 to November 2023 at Jiangsu Provincial Hospital of Traditional Chinese Medicine. The exposure of this study was who took the XHP. We assessed the efficacy of the XHP on MASLD by comparing FibroScan parameters, body composition indicators, and liver serological indicators. The XHP was then evaluated for MASLD by inverse probability of treatment weighting (IPTW) as well as log-binomial analysis. We ended up collecting the exposure cohort (n=163) and the referent cohort (n=99). Patients were categorized into an exposure cohort (n=163, XHP + basic treatment) subdivided by treatment duration: 4 weeks (n=28), 8 weeks (n=60), 12 weeks (n=51), and ≥16 weeks (n=24), and a referent cohort (n=99, basic treatment alone). The results showed significant improvements in Liver stiffness measurement (LSM), controlled attenuation parameter (CAP), body mass index (BMI), waist-to-hip ratio (WHR), visceral fat area (VFA), the fatty liver index (FLI), and FibroScan-AST (FAST) in the exposure cohort after treatment compared to before treatment. After controlling confounding by IPTW, log-binomial analysis revealed that XHP administration was significantly more effective for MASLD in the exposure cohort than in the referent cohort (weighted risk ratio=2.99, 95% CI=1.86 to 4.89, p<0.001). Subgroup analyses revealed a significantly greater efficacy of the XHP in the exposure cohort compared to the MASLD referent cohort, across various durations and dosages of XHP and varying degrees of hepatic steatosis and fibrosis. No serious adverse events occurred; occasional mild gastrointestinal reactions were self-limiting. The results of our study suggest that XHP has a significant treatment effect on MASLD, which hopes to complement the current lack of treatment for MASLD.

Rotenone and 6-hydroxydopamine are two drugs commonly used to generate Parkinson's disease animal models. They not only achieve degenerative changes of dopaminergic neurons in the substantia nigra, but also satisfy the requirements for iron deposition. However, few studies have compared the characteristics of these two models by magnetic resonance imaging. In this study, rat models of Parkinson's disease were generated by injection of 3 μg rotenone or 10 μg 6-hydroxydopamine into the right substantia nigra. At 1, 2, 4, and 6 weeks after injection, coronal whole-brain T2-weighted imaging, transverse whole-brain T2-weighted imaging, and coronal diffusion tensor weighted imaging were conducted to measure fractional anisotropy and T2* values at the injury site. The fractional anisotropy value on the right side of the substantia nigra was remarkably lower at 6 weeks than at other time points in the rotenone group. In the 6-hydroxydopamine group, the fractional anisotropy value was decreased, but T2* values were increased on the right side of the substantia nigra at 1 week. Our findings confirm that the 6-hydroxydopamine-induced model is suitable for studying dopaminergic neurons over short periods, while the rotenone-induced model may be appropriate for studying the pathological and physiological processes of Parkinson's disease over long periods.