Abstract:G protein-coupled receptor 5 (TGR5) is recently discovered to be a new membrane receptor that can regulate inflammation and metabolism. TGR5 activation can inhibit foam cell formation and atherosclerotic plaque rupture by reducing inflammation reaction, promote NO, H2S and other endogenous gas signal molecules to improve vascular endothelial dysfunction. In addition, it also can reduce atherosclerosis risk factors such as obesity and diabetes. Therefore, TGR5 may be an important target for prevention and treatment of atherosclerosis.

Abstract:Aim To investigate the nenuroprotective effects of hydrogen-rich saline on brain injury of acute carbon monoxide （CO） poisoned rats. Methods Adult male Sprague-Dawley rats were randomly assigned to the following groups: normal group, CO＋saline group and CO＋hydrogen salinegroup. Hydrogen-rich saline or normal saline was given intraperitoneally in the dose of 10 mg/kg with an interval of 8 hours for six consecutive times. The normal group rats were used as normal controls. At 5 days after CO poisoning, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay （TUNEL） staining, the activity of caspase-3, superoxide dismutase （SOD） and the content of malondialdehyde （MDA）, the level of tumor necrosis factor-α （TNF-α）, interleukin-6 （IL-6） and 8-oxo-7,8-dihydro-2′deoxyguanine （8-OHdG） were conducted in established acute carbon monoxide poisoned rats. Results TUNEL-poisitive cells, the content of MDA, the level of TNF-α, IL-6 and 8-OHdG, decreased the activity of caspase-3 and SOD were apparently reduced by hydrogen-rich saline. Conclusion Hydrogen-rich saline reduced CO encephalopathy through its antioxidant, anti-apoptopic and anti-inflammatory actions.

Abstract:Lipid accumulation and inflammatory reaction play a key role in the process of atherosclerosis, which promote and influence each other. The Adipophilin as cytoplasmic lipid droplets of imperfect-coating protein, not only can be used as a marker of atherosclerotic lipid accumulation, but also can promote lipid accumulation, and inhibit the efflux of intracellular cholesterol, and mediate the secretion of some inflammatory mediators, such as TNF-α, MCP-1 and IL-6, and its expression is regulated by various factors, like the nuclear receptors, fatty acid, modified lipoprotein and hormone-like substance. The purpose of this paper is to make an overview of how Adipophilina plays a role in lipid accumulation and inflammatory response in　order to help find a new thought about preventing Atherosclerosis through regulating.

Abstract:Aim To discuss the correlation of the polymorphism of tumor necrosis factor receptor superfamily 1B (TNFRSF1B) in the 196ed gene (T mutation for G) to the inflammation reaction mediated by the macrophage TNF-TNFR2 signaling pathways.Methods Genetic recombination technology was used to bulid eukaryotic expression vector pcDNA6.0-TNFR2196Met and pcDNA6.0-TNFR2196Arg, together with pcDN6.0 being transferred to macrophage by liposome transfection method respectively. In order to establish stable transfection cell lines, blasticidin was used to select them for 4 weeks after transfected 48 h. Digest the macrophages by pancreatic enzyme and divide them into four groups: control group, pcDNA6.0 empty plasmid group, pcDNA6.0-TNFR2196Met group and pcDNA6.0-TNFR2196Arg group. TNFR2, cIAP1, cIAP2 mRNA were detected by RT-PCR, the expression of p-JNK, cIAP1, cIAP2, TNFR2 and NF-κB were detected by Western blot, the level of sTNFR2, IL-1β and IL-6 in cell supernatant fluid were detected by ELISA.ResultsTNFR2 gene 196Met and 196Arg expression vector were successfully constructed which was verified by enzyme sequencing method. After transfected to marcophages, TNFR2, cIAP1, cIAP2, IL-1β, IL-6 and p-JNK expression were increased (P<0.05) in TNFR2196Arg and TNFR2196Met overexpression group compared with the blank control group and empty plasmid group. Each index decreased obviously in mutant TNFR2196Arg cell group compared with TNF2196Met cell group, especially,the reduction of NF-κB activity mediated by TNFR2196Arg was significant. Conclusions Successfully building stable expression TNFR2196Arg and TNFR2196Met vector will lay the foundation for the next inflammation research. The mutation of TNFR2 mediates inflammatory disease through TNF/TNFR2 signaling pathways, which is molecular mechanism of chronic inflammatory disease.