目的探讨紫杉醇能否预防心肌细胞线粒体缺血再灌注损伤,并对其机制进行初步探讨。方法将离体大鼠心脏分为对照组、缺血组、缺血+0.1μmol/L紫杉醇组、缺血+0.3μmol/L紫杉醇组和缺血+1μmol/L紫杉醇组(n=15)。每组先给予15 min平衡后,对照组继续给予150 min常氧灌注;缺血组给予30 min缺血处理(Langendorff灌流,结扎左前降支30 min)+120 min常氧再灌注;缺血+0.1μmol/L(或0.3μmol/L、1μmol/L)紫杉醇组给予30 min缺血处理+120 min常氧再灌注,整个过程中均给予0.1μmol/L(或0.3μmol/L、1μmol/L)紫杉醇灌流。灌流结束后,左心室心肌进行冰冻切片。采用免疫组织化学方法观察微管;DCFH-DA试剂盒用来检测活性氧物种的数量,同时通过荧光光度计和分光光度计检测氧化酶活性。结果 10.1μmol/L紫杉醇灌流能明显降低微管断裂评分。20.1μmol/L,0.3μmol/L和1μmol/L紫杉醇减少氧自由基水平分别为33%、46%和51%(P<0.05)。30.3μmol/L和1μmol/L紫杉醇增加线粒体电子传递链复合体Ⅰ的活性,而0.1μmol/L,0.3μmol/L和1μmol/L紫杉醇均增加线粒体电子传递链复合物Ⅲ的活性。结论紫杉醇能预防心肌细胞线粒体缺血再灌注损伤。减少氧自由基生成、增加线粒体电子传递链复合体Ⅰ、Ⅲ的活性或许是其作用机制之一。 Objective To investigate whether paclitaxel can prevent myocardial mitochondrial ischemia-reperfusion injury and to explore its mechanism. Methods The isolated rat heart was divided into control group, ischemia group, ischemia + 0.1μmol / L paclitaxel group, ischemia + 0.3μmol / L paclitaxel group and ischemia + 1μmol / L paclitaxel group (n = 15). The rats in each group were given 15 minutes of equilibration. The rats in the control group were given 150 minutes of normal oxygen perfusion. The rats in the ischemic group were given 30 minutes of ischemia (Langendorff perfusion and ligation of the left anterior descending artery for 30 minutes) Rats in the 0.1 mol / L (or 0.3 mol / L, 1 mol / L) paclitaxel group were given 30 min reperfusion with +120 min ischemia reperfusion. 0.1 μmol / L paclitaxel Paclitaxel perfusion. After perfusion, the left ventricular myocardium was frozen sectioned. Microtubules were observed by immunohistochemical method. DCFH-DA kit was used to detect the amount of reactive oxygen species. At the same time, the oxidase activity was detected by fluorophotometer and spectrophotometer. Results 10.1μmol / L paclitaxel perfusion can significantly reduce the microtubule fracture score. The levels of oxygen free radicals of 20.1μmol / L, 0.3μmol / L and 1μmol / L paclitaxel were 33%, 46% and 51%, respectively (P <0.05). Paclitaxel at 30.3μmol / L and 1μmol / L increased the activity of mitochondrial electron transport chain complex Ⅰ, while 0.1μmol / L, 0.3μmol / L and 1μmol / L paclitaxel increased the activity of mitochondrial electron transport chain complex Ⅲ. Conclusion Paclitaxel can prevent myocardial mitochondrial ischemia-reperfusion injury. Reduce the generation of oxygen free radicals and increase the activity of mitochondrial electron transport chain complex Ⅰ, Ⅲ may be one of the mechanisms of action.