| HMG-CoA Reductase Inhibitors(HRI), the so-called statins were most typical and effective class of lipid-lowering agents. Since their available for clinic use, great progress have been made in decreasing incidence of vascular atherosclerosis diseases. Treatment with HRI in a variety of experimental models of renal disease clearly demonstrated a renal protective effect by reducing proteinuria and ameliorating renal injury. HRI may have important effects on the renal structure by reducing glomerular mesangial cell proliferation, monocyte infiltration and mesangial matrix expansion. Being a tightly correlation between the progression of renal disease and dyslipidemia, this beneficial effects of HRI were generally attributed to their cholesterol lowering activity several years ago. However recent data from animal experiment without cholesterol changes have shown that HRI may exhibit renal protection independent of their effect on lipids regulation. The exact effect and mechanism of HRI on kidney had still not been fully elucidated. The aim of this study was to observe the direct effect of lovastatin on proliferation and secretion of HMC in vitro, and through observion of the regulatory effect of lovastatin on NF- κ B activity in HMC at the same time, we try to investigate the effective mechanism of lovastatin on HMC.METHOD: The DNA synthesis of HMC was measured by 3H-thymidine uptake. HMC cell cycle was measured by flow cytometric analysis. Using the methods of RT-PCR, we detected the proimflammtary cytokines mRNA expression in HMC after the stimulation by LPS. When HMC were incubated with varing concentrations of Lovastatin under LPS stimulated condition, The IL-6 in the supernatants was determined by RIA. The influence of Lovastatin on activation of NF- κ B in HMC after the stimulation by LPS were measured by EMSA. RESULT: Incubation with HMC for 48 hours, Lovastatin caused a significant dose-dependent reduction in 3H thymidine incorporation, (Lov 10-5, 10-6, 10-...
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