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Purpose : observe fluorine cutting his Ting hemolytic phosphatidyl choline damage human umbilical vein endothelial cells of the protection role , to explore outside his statin lipid-lowering role of other anti- artery atherosclerosis hardening mechanism , to provide a new basis for the clinical application of his statin drug 's . Methods : Human umbilical vein endothelial cells until the cell growth to the integration of state with different concentrations ( 10 -7 < / sup> -10 -5 mol / L) of fluvastatin statins incubated for 20 minutes , then add the the lysophosphatidylcholine (5mg / L) for 24 hours , using a semi - quantitative reverse transcription - polymerase chain reaction (RT-PCR) detection of eNOS mRNA and MMP -9 mRNA expression , immune cells staining the assay NF - KBp65 , of ICAM- 1 , VCAM -1 protein expression , flow cytometry apoptosis detection rate , tetrazolium salt colorimetric test (MTT) cell viability colorimetric assay cells in each group superoxide dismutase (SOD), glutathione (GSH), lactate dehydrogenase (LDH) activity and malondialdehyde (MOA), nitric oxide (NO) content changes . Results: 1 lysophosphatidylcholine significantly induced endothelial cell MMP - 9 mRNA and of NF- KBp65 , ICAM -1 , VCAM -1 protein expression , inhibition of eNOS mRNA expression , lowering of SOD , GSH activity , NO content and cell viability , and significantly increased LDH activity, MDA content and promote apoptosis ; 2 , pre- application of different concentrations of fluvastatin intervention , in a dose -dependent inhibition of the effect ; 3, jointly with nitric oxide inhibitors L- arginine methyl ester (L-NAME) reduce NO synthesis inhibition of nitric oxide synthase , the partial lifting of the protective effect of fluvastatin . Conclusion: 1, lysophosphatidylcholine induces vascular endothelial cells to oxidative stress and inflammation , leading to endothelial cell dysfunction ; fluvastatin statins by promoting the release of NO a dose-dependent inhibition of lysophosphatidylcholine oxidative stress induced by oxygen free radical damage , reduce endothelial cells ; 3 , fluvastatin Ting promote the release of NO , inhibition of NF - KB activity reducing ICAM-1, VCAM-1 and MMP-9 expression , inhibition inflammatory response and stability of atherosclerotic plaque ; fluvastatin on endothelial cells protective effect in addition to its promotion of the release of NO , there may be other substances or signal transduction pathways involved.
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