Abstract：Objective: To determine whether the cardioprotection of hydroxysafflor yellow A (HSYA) against anoxia／reoxygenation injury is mediated by mitochondrial transmembrane pores. Method: Cardiomyocytes were isolated from male Sprague-Dawley rats. Cell viability was assessed by trypan blue exclusion and mitochondrial membrane potential was measured by loading with TMRE. The opening of mitochondrial permeability transition pore was determined spectrophotometrically. Result: Pretreatment with HSYA at 0.1 mmol／L for 5 min increased the cell viability against anoxia／reoxygenation injury and attenuated mitochondrial depolarization induced by anoxia／reoxygenation. In mitochondrial isolated from hearts pretreated with 0.1 mmol／L HSYA for 5 min, a significant inhibition of Ca2+ induced swelling was observed, while NG-nitro-L-argininemethyl ester (L-NAME), an inhibitor of NOS, abrogated the protective effects of HSYA. Conclusion: These findings indicate that HSYA protected cardiomyocytes against anoxia／reoxygenation injury via inhibited mitochondrial permeability transition pore opening, while nitric oxide may take a part in it.
刘伊娜, 朱健华, 吴翔, 王政华. 羟基红花黄色素A抗心肌细胞缺氧复氧损伤的线粒体相关机制[J]. 江苏大学学报:医学版, 2013, 23(4): 313-316.
LIU Yi-na, ZHU Jian-hua, WU Xiang, WANG Zheng-hua. Mitochondrial mechanism of cardioprotective effect of hydroxysafflor yellow A against anoxia／reoxygenation injury in rats. Journal of Jiangsu University(Medicine Edition), 2013, 23(4): 313-316.
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2013, Vol. 23 
