Relationships between sarcopenia, nutrient intake, and gut microbiota in Chinese community-dwelling older women.

BACKGROUND: The relationship among gut microbiota, sarcopenia components, and influencing factors in female sarcopenic patients has been poorly investigated. METHODS: Female participants completed questionnaires of physical activity and dietary frequency and were assessed for the presence of sarcopenia by the Asian Working Group of Sarcopenia 2019 (AWGS 2019) criteria. Fecal samples were collected from 17 sarcopenia and 30 non-sarcopenia subjects for 16S sequencing and short chain fatty acid (SCFA) detection. RESULTS: The prevalence of sarcopenia was 19.20% among 276 participants. The dietary protein, fat, dietary fiber, vitamin B1, niacin, vitamin E, phosphorus, magnesium, iron, zinc, and cooper intake of sarcopenia were all remarkably low. In addition, the richness of gut microbiota (Chao1 and ACE indexes) was considerably reduced in sarcopenic patients, and the sarcopenic gut microbiota and its metabolite were decreased in Firmicutes/Bacteroidetes, Agathobacter, Dorea and Butyrate and were enriched in Shigella and Bacteroides. Correlation analysis showed that Agathobacter and Acetate were positively correlated with grip strength and gait speed, respectively, and Bifidobacterium was negatively correlated with grip strength and appendicular skeletal muscle index (ASMI). Moreover, the protein intake was positively related to Bifidobacterium. CONCLUSIONS: This cross-sectional study revealed the alterations of gut microbiota composition, SCFA, and nutrient intake in women with sarcopenia and their relation to sarcopenic components. These results provide insights into further studies on the role of nutrition and gut microbiota in sarcopenia and its use as a therapeutic approach.

Correlation between eating behaviors with body composition among medical students / 中国学校卫生

Objective@#To investigate the correlation between body composition and eating habits among medical students, and to provide evidence for health promotion.@*Methods@#In December 2021, stratified cluster random sampling method was used to conduct a questionnaire survey and body composition assessment among 445 students in grade one to grade four in Jining Medical University.@*Results@#There were 152 girls (53.3%) and 45 boys (28.1%) with low skeletal muscle mass. Totally 167 students ( 37.5% ) had lower muscle mass, including 115 females (40.4%) and 49 males (30.6%). High body fat percentage was found in 259 (58.2%) students, including 179 females (62.8%) and 80 males (50.0%). There were 192 students (43.1%) with abnormal waist to hip ratio, with 139 females (48.8%) and 53 males (33.1%). In addition, emotional eating score of female students was significantly higher than that of male students(6.85±2.24, 6.11±2.69, t =2.96, P <0.05). Cognitive restricted eating was positively correlated with skeletal muscle mass and musde mass( r=0.13, 0.13, P <0.05). Emotional eating was positively correlated with body fat percentage, body fat and waist hip ratio( r =0.20, 0.20, 0.16, P <0.05). Unrestricted eating was positively correlated with body fat percentage, body fat and waist hip ratio( r =0.15, 0.18, 0.15, P <0.05). Multiple linear regression analysis showed that gender, family residence, physical activity and cognitive eating were associated with skeletal muscle mass and muscle mass of medical students( P <0.05).@*Conclusion@#With low skeletal muscle mass, low muscle mass, body fat percentage and waist and hip high ratio, reasonable eating habits combined with resistance exercise should be adopted to improve their physical health.

Fecal microbiota transplantation ameliorates stress-induced depression-like behaviors associated with the inhibition of glial and NLRP3 inflammasome in rat brain.

BACKGROUND: Evidence from previous studies has demonstrated that the gut-microbiota-brain axis is vital in regulating of behavior and neuroinflammation in the central nervous system. Considering the putative connection among gut microbiota, neural function, and behavior, the present study investigated the potential signaling of gut microbiota to modulate depression-like behaviors and neuroinflammation. METHODS: Rats showing depression-like behaviors induced by chronic unpredictable mild stress received fecal microbiota treatment or vehicle for 14 days, and alterations in behavior and neuroinflammation were assessed. ELISA, immunofluorescence staining and Western blot were used to analysis the activation of glial cells and NLRP3 inflammasome. RESULTS: Treatment with fecal microbiota transplantation ameliorated depression-like behaviors. 5-Hydroxytryptamine decreased in the chronic unpredictable mild stress rat model but significantly increased after fecal microbiota transplantation. The treatment with fecal microbiota transplantation decreased the production of IL-1ß and TNF-α. Moreover, fecal microbiota transplantation administration suppressed the activation of Iba1 positive microglia cells and GFAP positive astrocytes cells and reduced the expression of NLRP3, ASC, Caspase-1, and IL-1ß pathway in the prefrontal cortex and hippocampus. CONCLUSIONS: Fecal microbiota transplantation can improve depression-like behaviors induced by chronic unpredictable mild stress. The anti-depression effects of fecal microbiota transplantation were associated with the suppressed activation of glial cells and NLRP3 inflammasome in the brain.

Fecal microbiota transplantation ameliorates gut microbiota imbalance and intestinal barrier damage in rats with stress-induced depressive-like behavior.

The gut-microbiota-brain axis is the most important complex and bidirectional pathway between the gastrointestinal tract and the central nervous system. This study investigated the potential of microbe-induced gut-to-brain signaling to modulate the effect of stress on depressive-like behavior, intestinal barrier, and neuroinflammation. Result showed that fecal microbiota transplantation increased the consumption of sucrose solutions and decreased the immobility time in forced swimming test. This treatment also increased Firmicutes and decreased Bacteroidetes and Desulfobacterota at phylum levels; reduced the loss of villi and epithelial cells; suppressed the inflammatory cell infiltration in the ileum; increased the expression of ZO-1, occludin; protected the mucosal layer function; and suppressed the high levels of inflammasomes (NLRP3, ASC, caspase-1, and IL-1ß) in rat brain. In summary, fecal microbiota transplantation improves the depressive-like behavior, alters the gut microbiota imbalance, and alleviates the intestinal tract inflammation, intestinal mucosa disruption, and neuroinflammation in rats induced by chronic unpredictable mild stress.

The role of macrophage-derived TGF-ß1 on SiO2-induced pulmonary fibrosis: A review.

Silicosis is an occupational fibrotic lung disease caused by inhaling large amounts of crystalline silica dust. Transforming growth factor-ß1 (TGF-ß1), which is secreted from macrophages, has an important role in the development of this disease. Macrophages can recognize and capture silicon dust, undergo M2 polarization, synthesize TGF-ß1 precursors, and secrete them out of the cell where they are activated. Activated TGF-ß1 induces cells from different sources, transforming them into myofibroblasts through autocrine and paracrine mechanisms, ultimately causing silicosis. These processes involve complex molecular events, which are not yet fully understood. This systematic summary may further elucidate the location and development of pulmonary fibrosis in the formation of silicosis. In this review, we discussed the proposed cellular and molecular mechanisms of production, secretion, activation of TGF-ß1, as well as the mechanisms through which TGF-ß1 induces cells from three different sources into myofibroblasts during the pathogenesis of silicosis. This study furthers the medical understanding of the pathogenesis and theoretical basis for diagnosing silicosis, thereby promoting silicosis prevention and treatment.

Based on Network Pharmacology to Explore the Molecular Targets and Mechanisms of Gegen Qinlian Decoction for the Treatment of Ulcerative Colitis.

BACKGROUND: Gegen Qinlian (GGQL) decoction is a common Chinese herbal compound for the treatment of ulcerative colitis (UC). In this study, we aimed to identify its molecular target and the mechanism involved in UC treatment by network pharmacology and molecular docking. Material and Methods. The active ingredients of Puerariae, Scutellariae, Coptis, and Glycyrrhiza were screened using the TCMSP platform with drug-like properties (DL) ≥ 0.18 and oral availability (OB) ≥ 30%. To find the intersection genes and construct the TCM compound-disease regulatory network, the molecular targets were determined in the UniProt database and then compared with the UC disease differential genes with P value < 0.005 and ∣log2 (fold change) | >1 obtained in the GEO database. The intersection genes were subjected to protein-protein interaction (PPI) construction and Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. After screening the key active ingredients and target genes, the AutoDock software was used for molecular docking, and the best binding target was selected for molecular docking to verify the binding activity. RESULTS: A total of 146 active compounds were screened, and quercetin, kaempferol, wogonin, and stigmasterol were identified as the active ingredients with the highest associated targets, and NOS2, PPARG, and MMP1 were the targets associated with the maximum number of active ingredients. Through topological analysis, 32 strongly associated proteins were found, of which EGFR, PPARG, ESR1, HSP90AA1, MYC, HSPA5, AR, AKT1, and RELA were predicted targets of the traditional Chinese medicine, and PPARG was also an intersection gene. It was speculated that these targets were the key to the use of GGQL in UC treatment. GO enrichment results showed significant enrichment of biological processes, such as oxygen levels, leukocyte migration, collagen metabolic processes, and nutritional coping. KEGG enrichment showed that genes were particularly enriched in the IL-17 signaling pathway, AGE-RAGE signaling pathway, toll-like receptor signaling pathway, tumor necrosis factor signaling pathway, transcriptional deregulation in cancer, and other pathways. Molecular docking results showed that key components in GGQL had good potential to bind to the target genes MMP3, IL1B, NOS2, HMOX1, PPARG, and PLAU. CONCLUSION: GGQL may play a role in the treatment of ulcerative colitis by anti-inflammation, antioxidation, and inhibition of cancer gene transcription.

Association of lymphoid tissue-resident commensal bacteria in mice with depressive-like behaviors induced by chronic social defeat stress.

Emerging evidence suggests that the microbiota-gut-brain axis affects a variety of complex behaviors, including social, emotional, and depressive-like behaviors. Peyer's patches (PPs), a well-characterized gut-associated lymphoid tissue, are the entry site for luminal antigens and the initiation site for antigen-specific immune responses. However, few studies have explored the composition of lymphoid tissue-resident commensal bacteria (LRCs) in stress-associated disorders. Male C57BL/6 mice exposed to chronic social stress were analyzed for microbiome on the interior of PPs and changes in inflammation. Susceptible mice (SUS) exhibited a composition of bacteria inside PPs that was distinct from that of control (CON) and resilient (RES) mice, including an increase in Candidatus Arthromitus (SFB) and a decrease in Lactobacillus. The CD4+ CD25+ Foxp3+ T cells were significantly reduced in SUS mice. Relative mRNA levels of IL-2 were significantly reduced in SUS mice, and the mRNA levels of Bcl-6, IFN-γ, IL-6, and the IgA protein levels in the ileum were significantly increased. Moreover, in the prefrontal cortex of SUS mice, IL-6 and TNF-α were increased, whereas IL-10 was decreased. The correlational analyses revealed that social interaction ratio was negatively correlated with SFB and positively associated with Lactobacillus and four other candidate protective organisms. These results pointed the possibility that the changes in the LRCs induced by chronic social defeat stress were ultimately associated with the inflammation of the brain and exacerbation of depressive-like behaviors.

Oral treatment with Lactobacillus reuteri attenuates depressive-like behaviors and serotonin metabolism alterations induced by chronic social defeat stress.

BACKGROUND: Alterations in bidirectional gut-brain interactions are believed to be involved in the pathogenesis of neuropsychiatric diseases. Considering the putative connections among gut microbiota, neural function, and behavior, this study investigated the potential of microbe-induced gut-to-brain signaling to modulate the impact of stress on depressive-like behaviors and serotonin metabolism. METHODS: Depression-susceptible mice induced by chronic social defeat stress received oral treatment of either Lactobacillus reuteri 3 (L. reuteri 3) or vehicle for 28 days, and alterations in behavior and serotonin metabolism were assessed. 16S rRNA sequencing and gas chromatograph were employed to analyze the gut microbiota community and short-chain fatty acids (SCFAs). RESULTS: Treatment with L. reuteri 3 ameliorated depressive-like behaviors, suppressed the increase in the relative abundances of Clostridiales and Adlercreutzia, improved the decrease in abundances of Lactobacillus, Allobaculum, and Sutterella induced by stress, and significantly increased the proportion of Bifidobacterium. L. reuteri 3 reduced the acetate and total SCFAs levels in the depression group. Blood and colon 5-HT were decreased in depressive-like mice but were significantly ameliorated after L. reuteri 3 treatment. Moreover, L. reuteri 3 administration increased the expression of enzymes involved in serotonin biosynthesis but suppressed that of the enzymes involved in tryptophan metabolism along the kynurenine pathway in colon and prefrontal cortex. CONCLUSIONS: Despite the complexity of the gut microbiota, exposure to a single microbial strain L. reuteri 3 can protect against depressive-like behaviors induced by chronic social defeat stress. The anti-depressive effects of L. reuteri 3 were associated with improved gut microbiota and serotonin metabolism.

The involvement of autophagic flux in the development and recovery of doxorubicin-induced neurotoxicity.

Doxorubicin (Dox) is an effective anti-cancer agent, whose clinical use is limited by the cytotoxicity in non-target tissues, especially the heart and brain. The drug-induced neuronal damage is primarily mediated by oxidative stress, in which autophagy plays a central role. Although numerous studies indicate the involvement of autophagy in neurodegenerative diseases and brain injury, the evidence concerning autophagic process in Dox-induced neuronal death is limited. We found that repeated Dox administration induced the protein expression of LC3II and P62 and impaired autophagic flux with enhanced autophagasome accumulation in rat hippocampus, whereas two weeks after the cessation of Dox treatment, the autophagic process was restored, even stimulated, with normalized protein levels of LC3II and P62 and enhanced expression of Becline-1, indicating a compensatory response in the recovery state. Likewise, while repeated Dox exposure inhibited the hippocampal expression of lysosomal-associated membrane protein 2 (LAMP2) and cathepsin D (CTSD), and suppressed CTSD activity, the Dox-induced impaired autophagy-lysosome pathway was also restored in rats following two weeks of recovery. To further verify the role of autophagy, the autophagy inhibitor, 3-methyladenine (3-MA), was administrated daily for the two weeks of recovery period. Our data demonstrated that while the animals in the recovery state showed a significant trend to decreased oxidative damage, normalized antioxidative system and ameliorated endoplasmic reticulum (ER) stress compared with Dox-induced toxic model, 3-MA treatment abrogated the recovering process, resulting in sustained oxidative and ER stress and neuronal apoptosis. Collectively, the present study firstly provided the evidence for the involvement of autophagy in both development and recovery of Dox-induced neurotoxicity, highlighting a novel target for mitigating the chemotherapy-induced neuronal damage.

The Association Between Vitamin D Binding Protein Polymorphisms and Vitamin D Level on Epilepsy in China.

Accumulating studies suggest the potential association between epilepsy and vitamin D (VD) in recent years. Vitamin D binding protein (VDBP) is the main VD carrier and can affect the availability of VD and its metabolites. Thus, this study aimed to investigate the association between VDBP polymorphisms and VD level on epilepsy. A total of 220 epilepsy patients and 210 health controls were enrolled and polymorphisms of VDBP (rs4588, rs7041, rs2298849, and rs2282679) genotype were detected using the PCR-ligase detection reaction method. The circulating status of VD metabolites, 25(OH)D and 24,25(OH)2D, was detected by a validated high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS) method, and the VD metabolite ratio (VMR), 24,25(OH)2D:25(OH)D, was then calculated. The frequency of rs4588(C>A) and rs2282679(A>C) genotype with AC was significantly lower among the patients relative to the controls [odds ratio, OR = 0.597, 95% confidence interval, CI = 0.401-0.890, p = 0.011 for rs4588(C>A); OR = 0.611, 95% CI = 0.409-0.912, p = 0.016 for rs2282679(A>C), respectively]. For rs7041 genotype distribution, VMR level was significantly higher in patients with GG genotype than in those carrying TT and TG genotype (p = 0.008). Our study demonstrated that the polymorphisms of VDBP rs4588 and rs2282679 may play a potentially important role in epilepsy susceptibility in Chinese Han population.