Visfatin Enhances ICAM-1 And VCAM-1 Expression Under Lps Treatment In Rat Cadiocyte

Recently, we can find lots of reports about LPS or Visfatin to induce cell damage. However, we do not discover both of them to influence the development of inflammation in myocardium. Here, we investigated the effect of visfatin on the treatment of LPS in mycardium. [Background]:Visfatin has recently been identified as a novel visceral adipokine which may be involved in obesity-related vascular disorders. It also functions as a proinflammatory adipocytokine. Lipopolysaccharides (LPS) are the key components of the outer membranes of gram-negative bacteria and have been shown present in the organic dusts, one of the major candidates for inflammatory reaction. [Experiment Principle]:LPS inflammatory models in adding Visfatin, extracellular stimulus makes I-κB kinase complex activative, making the phosphorylated form of cell plasma deposited in the NF-κB and I-κB complex separation, NF-κB exposure sites, free of verification a rapid shiftκB-NF, get into the nucleus, combined with specificityκB series, induction related gene transcription, cause adhesion factor ICAM- 1 and VCAM- 1 the expression of white blood cells, inducing gathered and adhesion; led to various inflammatory factor expression, resulting in myocardial injury. [Metheds]:MTT,RT-PCR,Western blot.[Experimental result]:LPS and visfatin induced the myocardium by induction of the cell adhesion molecules, ICAM-1 and VCAM-1. Promoter analysis revealed that LPS and visfatin mediated induction of CAMs is mainly regulated by nuclear factor-kB (NF-κB). The stimulus leads I-κB phosphorylation, nuclear translocation of the P65 subunit of NF-κB, and NF-κB DNA binding activity in cadiocyte. Both of them induce adhesion of leukocytes to endothelial cells. Finally, myocardial damage generated.Conclusions:LPS, Visfatin can increase ICAM-1 and VCAM-1 expression in myocardial cells. Both of them induce the promoter activity of ICAM-1 and VCAM-1 genes through NF-κB.