摘要
目的:观察丹参酮ⅡA对自发性高血压大鼠(SHR)左心室谷胱甘肽-s-转移酶μ2(glutathione-s-transferase μ2,GSTμ2)表达的影响,探讨丹参酮ⅡA防治左心室肥厚的机制。方法:实验分3组:(1)正常对照组;(2)SHR组;(3)丹参酮ⅡA组。处理后检测血流动力学指标、左室重量指数及大鼠左心室GSTμ2的活性,采用共聚焦显微镜检测左心室O2.-的产生情况,Western blotting检测GSTμ2的表达情况。结果:SHR组血压与左室重量指数均显著高于正常对照组,左心功能明显下降;丹参酮ⅡA显著逆转了SHR的左心室肥厚,但未明显改善高血压。SHR组左心室O2.-的产生较正常对照组显著增多,而丹参酮ⅡA治疗后,O2.-产生较SHR组显著减少。GSTμ2的表达及活性在SHR组显著降低,而丹参酮ⅡA显著增加了GSTM2的表达及活性。结论:丹参酮ⅡA能逆转SHR的左心室肥厚,这可能与其增加GSTμ2表达,减少活性氧产生,消除氧化应激有关。
AIM： To observe the effects of tanshinone Ⅱ A on the expression of glutathione-s-transferase μ2 （GSTμ2） in spontaneously hypertensive rats, and to investigate the mechanism of the reversal of left ventricular hypertrophy by tanshinone Ⅱ A. METHODS： There are 3 groups in the experiment： control, spontaneously hypertensive rats（SHR）, SHR treated by tanshinone Ⅱ A. At the endpoint of the experiment, hemodynamic parameters were measured. Then the rats were sacrificed, body weight （BW） and left ventricular weight （LVW） were measured, and the LVW/BW ratios were calculated. The oxidative fluorescence dye dihydroethidium was determined by laser confocal fluorescent microscopy to evaluate in situ O2^.- generation in the left ventricles. The expression of GSTμ2 was investigated by western blotting. RESULTS： Compared with control, the systolic blood pressure and LVW to BW ratios of SHR elevated markedly, the left ventricular function was decreased. The left ventricular hypertrophy was significantly reversed by tanshinone Ⅱ A treatment, but tanshinone Ⅱ A didn＇t decrease the systolic blood pressure of SHR. O2^.- generation increased in SHR significantly, and it was decreased by tanshinone Ⅱ A. The expression and activities of GSTμ2 in left ventricular significantly decreased in SHR, however that was reversed by tanshinone Ⅱ A. CONCLUSION： Tanshinone Ⅱ A can significantly reverse the left ventricular hypertrophy in SHR, that might be associated with up-regulation of GSTμ2, decrease of O2^.- and elimination of oxidative stress.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2008年第1期57-61,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
国家自然科学基金资助项目(30672459)
广东省医学科研课题资助项目(A2007309)
广东药学院博士启动科研课题资助项目(43540140)
