The Injury Of CSE On The Huves And The Intervention By Atorvastatin

Background: peripheral vascular ischemic disease such asatheroscleros（AS）, thromboangiitis obliterans(TAO) is common disease invascular surgery, its pathogenesis is not clear, Treatment effect is not ideal,especially with thromboangiitis obliterans. Smoking is an important riskfactor in the onset and development of such disease。Usually the initiatefactors of the disease is endothelial cell injury, therefore, explore theendothelial cell injury by smoking can helps us to understand themechanism of this kind of disease. In this paper，we use the method of cellculture in vitro to explore the endothelial cell injury by cigarette extract,and also explore the effect of intervention to the injury by atorvastatin，inorder to offer new ideas and approaches for the prevention and treatment.Objective: To investigate the effects of atorvastatin on the cellmorphology,levels of nitrogen oxide (NO)、 levels of endothelialnitricoxide synthasc(eNOS) and the expressions of intercellular adhesionmolecule （ICAM-1）of cultured human umbilical vein endothelialcells(HUVECs) injured by Cigarette smoking extract(CSE)．Methods: Isolated HUVECs were divided into normal control group, CSE group and CSE+atorvastatin group.In CSE+atorvastatingroup,cell were firstly incubated with atorvastatin for4hours, thenincubated with CSE.Cell morphology was observed by Invertedmicroscope, cell inhibition rate was detected by method of MTT, NO inthe supernatants of the cultures was assayed by nitrate reductasemethod,eNOS expressions were measured by Immune cells chemical，expressions of protein of ICAM-1were detected by Western blotting。Results: Compared with normal control group,the cell morphologywas much irregular, cell inhibition rate increased,the level of NO andeNOS were lower，the protein expressions of ICAM-1was obviouslyincreased in CSE group(p<0.05)． However， there was no obviousdifferences of the cell morphology, the level of NO and eNOS and proteinexpressions of ICAM-1between normal control group and CSE+atorvastatin group(p>0.05)．Conclusion: CSE can injure endothelial function of HUVES andAtorvastatin can protect from endothelial function by CSE, the mechanismmay be related to the cell growth, cell morphology，s change，theexpressions of eNOS and the release of NO，the protein expressions ofICAM-1.