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].

作者信息

Zhang Xiao-hui, Zhang Bin, Gong Pei-li, Zeng Fan-dian

机构信息

Department of Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China.

出版信息

Yao Xue Xue Bao. 2004 Jun;39(6):401-5.

PMID:15491093

Abstract

AIM

To study the protective effect of procyanidins from the seedpod of the lotus (LSPC) on myocardial ischemia and reperfusion in rats.

METHODS

Myocardial 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.

RESULTS

LSPC 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.

CONCLUSION

The 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.

摘要

目的

研究莲房原花青素（LSPC）对大鼠心肌缺血再灌注损伤的保护作用。

方法

采用结扎冠状动脉30分钟后再灌注45分钟的方法，建立麻醉大鼠心肌损伤模型；在离体大鼠心脏上，采用30分钟缺血后再灌注30分钟的方法。所有动物在实验前均给予药物或生理盐水。观察血清中内皮素（ET）、血管紧张素I（Ang I）、血管紧张素II（Ang II），丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性、一氧化氮（NO）水平，再灌注后冠状动脉血流量（CF）和心率（HR）的恢复率，以及心肌细胞中的肌酸激酶（CK）、黄嘌呤氧化酶（XO）。

结果

结果显示，LSPC能抑制ET、Ang II的释放（P<0.05），抑制MDA含量的升高（P<0.05）。还发现其能提高SOD活性（P<0.05）和NO水平（P<0.01）。LSPC能提高再灌注后冠状动脉血流量（CF）和心率（HR）的恢复率（P<0.05或P<0.01），减少心肌细胞中CK的释放（P<0.01），降低心肌组织XO活性（P<0.05），并改善心肌细胞超微结构病理损伤。