瑞舒伐他汀对高同型半胱氨酸血症大鼠主动脉Bcl-2与Bax表达的影响

Effects of rosuvastatin on Bcl-2 and Bax expressions in aorta of rats with hyperhomocysteinemia

摘要:

目的：观察瑞舒伐他汀对高同型半胱氨酸血症（hyperhomocysteinemia，Hhcy）Wistar大鼠主动脉组织B细胞淋巴瘤/白血病-2（B cell leukemia/lymphoma-2，Bcl-2）和B细胞淋巴瘤/白血病-2相关蛋白X（Bcl-2-associated X protein，Bax）表达的影响。方法：应用ADVIA2400全自动生化仪检测正常对照组，Hhcy组和瑞舒伐他汀组大鼠的血清甘油三酯、总胆固醇、低密度脂蛋白-胆固醇和血浆同型半胱氨酸（homocysteine，Hcy）浓度；HE染色观察主动脉病理变化；应用免疫组化和实时荧光定量PCR检测主动脉组织Bcl-2、Bax表达。结果：瑞舒伐他汀组大鼠血浆Hcy浓度（10.47±0.07） μmol/L低于Hhcy组（85.38±0.2） μmol/L，差异具有统计学意义（P<0.05）；瑞舒伐他汀组大鼠主动脉损伤较Hhcy组减轻；免疫组化显示瑞舒伐他汀组大鼠主动脉Bcl-2蛋白表达比Hhcy组降低，Bax蛋白表达比Hhcy组升高，差异均具有统计学意义（P<0.05）；实时荧光定量PCR法显示瑞舒伐他汀组大鼠主动脉Bcl-2 mRNA表达较Hhcy组明显降低，而Bax mRNA表达却升高（P<0.05）。结论：瑞舒伐他汀可能通过降低血浆Hcy浓度及影响主动脉组织Bcl-2、Bax基因表达，从而延缓和改善Hhcy大鼠主动脉粥样硬化的进程及程度。

Abstract:

Objective：To investigate the effects of rosuvastatin on expressions of B cell leukemia/lymphoma-2（Bcl-2） and Bcl-2-as－sociated X protein（Bax） in aortas of Wistar rats with hyperhomocysteinemia（Hhcy）. Methods：Serum triglyceride，total cholesterol，low density lipoprotein-cholesterol and plasma homocysteine（Hcy） concentrations were detected by ADVIA2400 automatic biochemi－cal analyzer，pathological changes of aorta were observed by HE staining and Bcl-2 and Bax expressions of aortic tissues were detect－ed by immunohistochemistry and RT-qPCR detection. Results：Plasma Hcy concentration was lower in rosuvastatin group than in Hh－cy group，（10.47±0.07） μmol/L vs. （85.38±0.2） μmol/L，with statistically significant differences（P<0.05）. Aortic injury was less se－vere in rosuvastatin group than in Hhcy group. Immunohistochemistry demonstrated that Bcl-2 protein expressions were lower in ro－suvastatin group than in Hhcy group and Bax protein expressions were higher in rosuvastatin group than in Hhcy group，with statisti－cally significant differences（P<0.05）. RT-qPCR assay showed Bcl-2 mRNA was decreased in rosuvastatin group than in Hhcy group and Bax mRNA was increased in rosuvastatin group than in Hhcy group（P<0.05）. Conclusions：Rosuvastatin can delay Hhcy rat aortic atherosclerosis hardening process through decreasing plasma Hcy concentration and influencing aortic tissue Bcl-2 and Bax gene ex－pressions.