金丝桃苷对大鼠心肌缺血再灌注损伤的保护作用

目的 探讨金丝桃苷（Hyp)对大鼠心肌缺血后再灌注导致的损伤的保护作用及作用的机制。方法 大鼠心肌缺血30min后再灌3.5h造成心肌缺血再灌注损伤模型；测定造模前腹腔注射Hyp对损伤大鼠心电图和血清中CPK及心肌组织中MDA，SOD和NO生成的影响。观察损伤大鼠心肌细胞凋亡的形成和Hyp干预的结果。结果 Hyp可以改变缺血再灌注损伤大鼠心电图T波的变化幅度，减少缺血再灌注损伤导致的大鼠心律失常发生率，抑制大鼠血清CPK的程式高和心肌组织中MDA，NO的形成，提高SOD的活力；抑制损伤大鼠心肌细胞凋亡的发生。结论 Hyp可以减轻大鼠心肌缺血再灌注损伤和心肌细胞凋亡。作用的机制可能与其抗氧自由基和NO自由基的形成，减少心肌缺血再灌注凋亡的发生有关。

Protective effects of hyperin against ischemia/reperfusion injury in rats

OBJECTIVE The effect and mechanism of hyperin(Hyp) against myocardium injury induced by ischemia and reperfusion in rats was studied.METHODS The injured model was established by ischemia 30 min and reperfused 3.5 h in male rats by LAD occlusion.Hyp was administered by ip before the model established.Then the electrocardiogram (ECG) and creatine phosphokinase(CPK) in serum were observed.The malondialdehyde(MDA),superoxide dismutase(SOD) and NO of myocardium in rats were also measurated.The effect of Hyp against cardiomyocyte apoptosis was observed.RESULTS The results showed that Hyp reduced the T wave change range,decreased the MDA contents( P <0.05),improved the SOD activities( P < 0.01 ),inhibited the nitric oxide (NO) production( P <0.05, P <0.01) on myocardium and also decreased the production of CPK in serum on ischemia/reperfusion rats( P <0.05, P <0.01) respectively.Hyp also decreased the number of apoptotic cells in myocardium injured by ischemia/reperfusion in rats( P <0.01).CONCLUSION Hyp showed protective effect against myocardial ischemia and reperfusion injured,to resist the damaging of oxygen free radical( OFR) and NO free radical,and decreased the amount of apoptotic cells of myocardium induced by ischemia and reperfusion in rats.