海胆黄多糖SEP抑制高糖高胰岛素诱导的大鼠乳鼠心肌细胞肥大

摘要

Aim To study the protective effects of SEP on the hypertrophic myocardial cells induced with high glucose and high insulin and the mechanism. Methods The protein content was assayed with Lowrys meth-od;the cardiomyocytes area was measured by computer photograph analysis system;the expression of ANF and PPAR-α was determined by RT-PCR;APS was select-ed as control drug. Results Compared with conctrol group,the protein content,cardiomyocytes area and the expression of ANF and PPAR-α of high glucose and high insulin group were significantly increased. Com-pared with conctrol group,the SEP of different dosages were able to decrease the protein content, area, the expression of ANF mRNA and PPAR-α mRNA of cul-tured hypertrophic myocadial cells induced with high glucose and high insulin. Conclusion SEP can pre-vent cardiomyocyte hypertrophy induced by high glu-cose and high insulin, which is related to its inhibition on PPAR-α signaling path.%目的：观察海胆黄多糖SEP对高糖高胰岛素诱导的肥大心肌细胞的影响,并初步探索其作用机制。方法利用高糖高胰岛素模拟糖尿病机体微环境诱导乳鼠心肌细胞肥大模型,选择不同剂量海胆黄多糖SEP分组给药处理后,采用Lowrys法检测心肌细胞蛋白质含量；利用计算机图像分析系统检测心肌细胞表面积变化；采用RT-PCR法检测给药前后心肌细胞ANF和PPAR-α mRNA表达变化。结果与正常对照组相比,高糖高胰岛素组蛋白含量、细胞表面积、ANF和PPAR-α mRNA表达均明显增加；与高糖高胰岛素组相比,低、中、高给药组剂量依赖性降低了高糖高胰岛素诱导的肥大心肌细胞的蛋白含量、细胞表面积、以及 ANF 和PPAR-α mRNA表达。结论 SEP对高糖高胰岛素诱导的乳鼠心肌细胞肥大具有一定的抑制作用,PPAR-α信号通路可能参与了这一过程。