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目的 探讨肿瘤坏死因子 α(TNF α)对肾小球前小动脉平滑肌细胞 (RASMC)Ⅰ型三磷酸肌醇 (IP3 )受体蛋白表达的影响。方法 通过对RASMC的分离、培养和鉴定 ,应用蛋白和核酸杂交技术分别检测TNF α作用后RASMC中Ⅰ型IP3 受体蛋白和Ⅰ型IP3 受体mRNA的表达情况 ,同时测定Ⅰ型IP3 受体mRNA的半衰期。结果 TNF α能增强RASMC内Ⅰ型IP3 受体蛋白的表达 ,且两者呈剂量依赖关系 ;TNF α能促进Ⅰ型IP3 受体mRNA的表达 ,同时使受体蛋白合成增加 ;而TNF α对Ⅰ型IP3受体mRNA的影响不是抑制mRNA的降解 ,而是使其表达增加。结论 TNF α可能作用于Ⅰ型IP3 受体mRNA的基因启动子 ,使其合成增加 ,由此导致Ⅰ型IP3 受体蛋白表达增加 ,诱导RASMC内储备的Ca2 + 释放至细胞浆 ,引起肾小球前小动脉平滑肌细胞收缩 ,使肾血流量减少 ,肾小球滤过率下降 ,从而导致肾功能异常
Objective To investigate the effect of tumor necrosis factor α (TNFα) on type Ⅰ inositol 1,4,5 - trisphosphate (IP3) receptor protein in glomerular prearterial artery smooth muscle cells (RASMC). Methods The expression of type Ⅰ IP3 receptor protein and type Ⅰ IP3 receptor mRNA in RASMC were detected by protein and nucleic acid hybridization after isolation, culture and identification of RASMC. The expression of type Ⅰ IP3 receptor mRNA Half-life. Results TNFα enhanced the expression of type Ⅰ IP3 receptor protein in RASMCs in a dose - dependent manner. TNFα promoted the expression of type Ⅰ IP3 receptor mRNA and increased the synthesis of receptor proteins. Type IP3 receptor mRNA does not inhibit the degradation of mRNA but instead increases its expression. Conclusions TNFα may act on the gene promoter of type Ⅰ IP3 receptor mRNA to increase its synthesis, leading to the increase of type Ⅰ IP3 receptor protein expression and the release of Ca2 + in RASMC to the cytoplasm, causing glomerular Contraction of the smooth muscle cells of the anterior small artery leads to a decrease in renal blood flow and a decrease in glomerular filtration rate, resulting in abnormal renal function