张晓晖, 张斌, 龚培力, 曾繁典. 莲房原花青素对大鼠心肌缺血再灌注损伤的保护作用J. 药学学报, 2004, 39(6): 401-405.
引用本文: 张晓晖, 张斌, 龚培力, 曾繁典. 莲房原花青素对大鼠心肌缺血再灌注损伤的保护作用J. 药学学报, 2004, 39(6): 401-405.
ZHANG Xiao-hui, ZHANG Bin, GONG Pei-li, ZENG Fan-dian. Protective effect of procyanidins from the seedpod of the lotus on myocardial ischemia and reperfusion injury in ratJ. Acta Pharmaceutica Sinica, 2004, 39(6): 401-405.
Citation: ZHANG Xiao-hui, ZHANG Bin, GONG Pei-li, ZENG Fan-dian. Protective effect of procyanidins from the seedpod of the lotus on myocardial ischemia and reperfusion injury in ratJ. Acta Pharmaceutica Sinica, 2004, 39(6): 401-405.

莲房原花青素对大鼠心肌缺血再灌注损伤的保护作用

Protective effect of procyanidins from the seedpod of the lotus on myocardial ischemia and reperfusion injury in rat

  • 摘要: 目的探讨莲房原花青素(LSPC)对大鼠心肌缺血再灌注损伤的作用。方法用麻醉大鼠冠脉结扎30 min后,再灌注45 min造成心肌损伤模型。离体大鼠心脏经停灌30 min后,用正常K-H液复灌30 min,造成心肌损伤模型。均于实验前给予药物或生理盐水。结果LSPC可降低复灌后血清ET和Ang II的浓度,抑制MDA含量升高,并保持SOD活性及NO的水平。心脏复灌以后冠脉流量和心率明显恢复,心肌细胞酶CK和LDH漏出减少,心肌组织黄嘌呤氧化酶(XO)的活性降低,心肌超微结构的病理变化改善等。结论LSPC对整体及离体大鼠心肌缺血再灌注损伤具有保护作用。

     

    Abstract: AimTo study the protective effect of procyanidins from the seedpod of the lotus (LSPC) on myocardial ischemia and reperfusion in rats. MethodsMyocardial injury model was made by ligating the coronary artery for 30 min followed by reperfusion for 45 min in anesthetized rat and 30 min of ischemia followed by 30 min of reperfusion in the isolated rat heart. All animals were given the medicine or normal saline before the experiment. ET, Ang I, Ang II in the serum, the MDA content, SOD activity, NO level, the recovery rate of coronary flow (CF) and heart rate (HR) after reperfusion and CK, XO from the myocardial cells were observed. ResultsLSPC was shown to inhibit the release of ET, Ang II (P﹤0.05), and the increase of MDA content (P﹤0.05). It was also found to increase the SOD activity (P﹤0.05) and NO level (P﹤0.01). LSPC was found to increase the recovery rate of the coronary flow (CF) and heart rate (HR) after reperfusion (P﹤0.05 or P﹤0.01), decrease the release of CK from the myocardial cells (P﹤0.01), depress the XO activity of myocardial tissue (P﹤0.05), as well as improve the myocyte ultrastructural pathological injury. ConclusionThe anti-ischemia effect of LSPC was related to the mechanism of scavenging the oxygen free radicals directly, cutting off the source of free radicals, reducing tissue peroxidation, stabilizing the cells membrane, depressing the production of EDCF and increasing the NO level as well.

     

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