摘要
目的观察阿托伐他汀(atorv)对氧化低密度脂蛋白(ox-LDL)诱导的人肾小球系膜细胞(HGMCs)增殖和转化生长因子β1(TGF-β1)mRNA及丝裂原活化蛋白激酶(p38MAPK)蛋白表达的影响。方法在体外培养HG-MCs,用MTT法检测细胞增殖,用半定量RT-PCR法检测细胞TGF-β1 mRNA表达,用Western blot法检测细胞p38MAPK蛋白合成。结果1.Ox-LDL(80μg/ml)刺激系膜细胞增殖;2.Ox-LDL(10μg/ml-80μg/ml)以浓度依赖的方式增加HGMCs TGF-β1 mRNA和p38MAPK蛋白表达,3.Atovastatin(6μg-12μg/ml)抑制系膜细胞增殖,降低ox-LDL引起的TGF-β1 mRNA表达上调,抑制p38MAPK信号途径激活。结论阿托伐他汀可能通过对抗p38MAPK信号通路,减少TGFβ1分泌,抑制ox-LDL引起的肾小球系膜细胞增殖,预防和治疗伴有血脂异常的糖尿病肾脏病变。
Objective 1. To observe the effect of atorvastatin on cell proliferation and expression of TGF-β1 mRNA and p38MAPK in human glomerular mesangial cells (HGMCs) induced by ox-LDL. Methods Cultured human glomerular mesangial cells were used. Cell proliferation was measured by MTT, TGF-β1 mRNA expression by RT-PCR, and p38MAPK protein expression in HGMCs by Western blot. Results 1. Ox-LDL (80μg/ml) stimulated mesangial cell proliferation; 2. Ox-LDL (10μg/ml-80μg/ ml) increased the expression of HGMCs TGF-β1 rnRNA in a concentration-dependent manner; 3. Atorvastatin (6μg/ml- 12μg/ml) inhibited mesangial cell proliferation and attenuated TGFβ1 mRNA and p38MAPK expression upregulation induced by Ox-LDL. Conclusion Atorvastatin may exert its beneficial effect by inhibiting mesangial cell proliferation and attenuating TGF-β1 mRNA and p38MAPK expressions in diabetic nephropathy.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2007年第1期57-61,共5页
Chinese Journal of Histochemistry and Cytochemistry
基金
辽宁省重点科技攻关项目(2001225004)
关键词
阿托伐他汀
细胞增殖
转化生长因子Β1
丝裂原活化蛋白激酶
人肾小球系膜细胞
Atorvastatin
Cell proliferation
Transforming growth factor β1
p38 mito-gen-activated protein kinases
Human glomerular mesangial cell