论文部分内容阅读
目的 :研究氯沙坦抑制氧化低密度脂蛋白 (oxLDL)诱导的血管内皮细胞凋亡及其介导机制。方法 :应用大鼠模型 ,低密度脂蛋白 (LDL)体内诱导血管内皮细胞凋亡 ,氯沙坦进行干预 ,观察其对LDL诱导血管内皮细胞凋亡的影响。TUNEL法检测凋亡细胞 ,比色法测caspase 3酶活性 ,SP免疫组化法分析p5 3蛋白的表达。结果 :LDL组与对照组比较血管内皮细胞凋亡数显著增加 ,caspase 3酶活性显著增高 ,p5 3蛋白表达增强 ;氯沙坦干预组与LDL组比较凋亡细胞数显著减少 ,caspase 3酶活性下降 ,p5 3蛋白表达降低。结论 :LDL可通过激活caspase 3酶及上调p5 3蛋白的表达诱导大鼠血管内皮细胞凋亡 ;氯沙坦可通过抑制caspase 3酶活性及下调p5 3蛋白表达抑制LDL诱导凋亡
AIM: To investigate the inhibitory effect of losartan on oxLDL-induced apoptosis of vascular endothelial cells and its mechanism. Methods: Rat models were induced by low density lipoprotein (LDL), and losartan was intervened to observe the effect of LDL on the apoptosis of vascular endothelial cells. Apoptotic cells were detected by TUNEL assay. The activity of caspase 3 was assayed by colorimetric assay. The expression of p5 3 protein was analyzed by SP immunohistochemistry. Results: Compared with the control group, the number of apoptotic cells in the LDL group was significantly increased, the activity of caspase 3 was significantly increased and the expression of p5 3 protein was increased. The number of apoptotic cells in Losartan group and LDL group was significantly decreased, and the activity of caspase 3 Decreased, p5 3 protein expression decreased. CONCLUSION: LDL can induce the apoptosis of rat vascular endothelial cells by activating the expression of caspase 3 and up-regulating the expression of p5 3 protein. Losartan inhibits the apoptosis of LDL-induced apoptosis by inhibiting the activity of caspase 3 and down-regulating the expression of p5 3 protein