摘要
目的 :探讨肾疏宁防治系膜基质硬化的细胞分子机制。方法 :应用细胞培养技术 ,进行肾小球系膜细胞培养 ,采取血清药理学方法 ,制备肾疏宁药物血清 ,并分为低、中、高三个剂量梯度 ,利用血管紧张素Ⅱ为刺激因子 ,在 4h、8h、16h、32h四个时间段观察肾疏宁药物血清对正常和病理状态下系膜细胞增殖和分泌系膜基质ColⅣ及FN的影响。应用MTT测定系膜细胞增殖 ,细胞ELISA测定ColⅣ及FN的含量 ,RT -PCR检测ColⅣ及FN的mRNA水平。结果 :血管紧张素Ⅱ能明显促进MC增殖和系膜基质中ColⅣ及FN的分泌 ,16h达到高峰 ,32h时呈下降趋势 ,肾疏宁血清中、高剂量组对ColⅣ及FN的分泌均有明显抑制作用 ,并呈现剂量依赖关系。RT -PCR结果也说明肾疏宁血清对正常和血管紧张素Ⅱ刺激下的MC分泌ColⅣ及FN的mRNA表达有下调作用。结论 :肾疏宁能明显抑制肾小球系膜基质中ColⅣ及FN的合成与分泌 ,并在基因水平上对其有影响作用。
Objective:To study the cellular and molecular mechanism of Shenshuning(SSN) in preventing mesangial sclerosis.Methods:Mesangial cells(MC) stimulated with angiotensin(ATⅡ) were cultured with different concentration of SSN pharmacological serum(2.5%,5%,10%)and with different duration(4 h,8 h,16 h and 32 h).MC proliferation,secretion of colⅣ or FN and mRNA expression were measured by MTT, ELISA and RT-PCR.Results:MC proliferation was inhibited by SSN pharmacological serum in a dose-dependent manner under normal and pathological condition. After stimulation of Angiotensin Ⅱ,the secretion of colⅣ and FN reached its peak at 16 h,and began to decline at 32 h. SSN inhi bited the secretion of ColⅣ and FN in a dose-dependent manner. SSN also inhibited the expression of ColⅣ and FN mRNA.Conclusion:SSN is an effective recipe in treating MsPGN.SSN can significantly inhibit the secretion of ColⅣ or FN and its mRNA expression in vitro, which may be the mechanism of SSN in prevention and treatment of glomerusclerosis in MsPGN.
出处
《中国中西医结合肾病杂志》
2003年第3期141-144,共4页
Chinese Journal of Integrated Traditional and Western Nephrology
