Ecological shifts of salivary microbiota associated with metabolic-associated fatty liver disease.

Introduction: Metabolic-associated fatty liver disease (MAFLD) is the most common chronic liver disease related to metabolic syndrome. However, ecological shifts in the saliva microbiome in patients with MAFLD remain unknown. This study aimed to investigate the changes to the salivary microbial community in patients with MAFLD and explore the potential function of microbiota. Methods: Salivary microbiomes from ten MAFLD patients and ten healthy participants were analyzed by 16S rRNA amplicon sequencing and bioinformatics analysis. Body composition, plasma enzymes, hormones, and blood lipid profiles were assessed with physical examinations and laboratory tests. Results: The salivary microbiome of MAFLD patients was characterized by increased α-diversity and distinct ß-diversity clustering compared with control subjects. Linear discriminant analysis effect size analysis showed a total of 44 taxa significantly differed between the two groups. Genera Neisseria, Filifactor, and Capnocytophaga were identified as differentially enriched genera for comparison of the two groups. Co-occurrence networks suggested that the salivary microbiota from MAFLD patients exhibited more intricate and robust interrelationships. The diagnostic model based on the salivary microbiome achieved a good diagnostic power with an area under the curve of 0.82(95% CI: 0.61-1). Redundancy analysis and spearman correlation analysis revealed that clinical variables related to insulin resistance and obesity were strongly associated with the microbial community. Metagenomic predictions based on Phylogenetic Investigation of Communities by Reconstruction of Unobserved States revealed that pathways related to metabolism were more prevalent in the two groups. Conclusions: Patients with MAFLD manifested ecological shifts in the salivary microbiome, and the saliva microbiome-based diagnostic model provides a promising approach for auxiliary MAFLD diagnosis.

[Influence of vitexin on the expression of inflammatory cytokines in dental pulp stem cells induced by lipopolysaccharide].

PURPOSE: To investigate the effect of vitexin (VTX) on the expression of inflammatory cytokines in human dental pulp stem cells(hDPSCs) induced by lipopolysaccharide(LPS), and to explore the underlying mechanism. METHODS: hDPSCs were isolated and cultured, and CCK-8 method was used to detect the effect of VTX on proliferation of hDPSCs. hDPSCs were randomly divided into 4 groups: blank group (without LPS and VTX)，LPS group (2 µg/mL LPS)，2 µg/mL LPS + 25 µmol/L VTX，2 µg/mL LPS + 50 µmol/L VTX. The cells of all groups were cultured for 48 h. The gene levels of IL-1ß， IL-6 and IL-8 in hDPSCs were detected by real time qPCR(RT-qPCR). The change of COX-2 and MAPKs signaling pathways were detected by Western blot. SPSS 16.0 software package was used for statistical analysis. RESULTS: When the VTX concentration was less than 200 µmol/L, the cell viability was not affected(P>0.05). VTX at 25 and 50 µmol/L significantly reduced LPS-induced expression of IL-1ß, IL-6 and IL-8 at gene levels and COX-2 at protein level (P<0.05). CONCLUSIONS: VTX significantly inhibited the activation of ERK and p38 signaling pathway. VTX can reduce LPS-induced inflammatory cytokine expression in hDPSCs via restraining the activation of ERK and p38 signaling pathway.

Platelet-derived microparticles are implicated in remote ischemia conditioning in a rat model of cerebral infarction.

AIM: Remote ischemic preconditioning protects against ischemic organ damage by giving short periods of subcritical ischemia to a remote organ. We tested the hypothesis that remote ischemic conditioning can attenuate cerebral stroke in a rat middle cerebral artery occlusion (MCAO) model by microparticles (MPs). METHODS AND RESULTS: MPs were extracted from healthy rats that underwent hindlimb ischemia-reperfusion preconditioning (RIPC), and were transfused into rats that had undergone MCAO without RIPC. The transfusion resulted in an increase in platelet-derived MPs in blood and reduction in infarction area, confirmed by both 2-3-5-triphenyltetrazolium chloride staining and magnetic resonance imaging, albeit to a lesser degree than RIPC itself. Behavioral tests (modified Neurological Severity Score [mNSS]) were calculated to judge the behavioral change. However, no significant difference was observed after MP transfusion in 24 h or the following consecutive 9 days. CONCLUSIONS: RIPC induces an increase in MPs, and platelet-derived MPs may confer at least part of the remote protective effect against cerebral ischemic-reperfusion injury.