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目的:研究巴戟天寡糖对大鼠心肌缺血再灌注损伤的影响。方法:将96只Wistar大鼠随机分为假结扎组、缺血再灌注模型组、阳性药物(地奥心血康)对照组和3个巴戟天寡糖不同剂量2.8g/(kg·d)、1.4g/(kg·d)、0.7g/(kg·d)的给药组,给药组每日灌胃给予相应剂量的巴戟天寡糖及地奥心血康药液,假结扎组、缺血再灌注模型组灌胃给予相应容积的蒸馏水,共7天。末次给药1小时后,各组动物均接受开胸,除假结扎组不结扎外,其他各组均结扎左冠状动脉前降支30min,再灌注90min。观察心律失常评分、心肌梗死面积、心肌超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)等的变化。结果:与缺血再灌注模型组相比,DK组、巴戟天寡糖2.8g/(kg·d)、1.4g/(kg·d)给药组心律失常评分显著降低,心肌梗死面积明显缩小,心肌中SOD、CAT、GSH-Px酶活性显著升高,而MDA含量则显著降低(P<0.01)。结论:巴戟天寡糖有保护大鼠心肌和抗心肌缺血再灌注损伤作用,其机制主要与其提高心肌抗氯化酶活性,减少脂质过氧化反应有关。
Objective: To study the effect of Morinda officinosa on myocardial ischemia-reperfusion injury in rats. METHODS: Ninety-six Wistar rats were randomly divided into three groups: sham ligation group, ischemia reperfusion group, positive drug (Dao AoXuekang) control group and three glycogen free glycosides 2.8g/(kg·d), 1.4g. In the (kg·d) and 0.7 g/(kg·d) groups, the dosage group was given intragastrically with the corresponding doses of Bajitian oligosaccharide and Dioxinxuekang liquid, and the pseudo-ligation group and ischemia reperfusion model. The group was given intragastrically distilled water for a total of 7 days. One hour after the last administration, all groups of animals received thoracotomy. In addition to the ligation group, all other groups were ligated with the left descending coronary artery for 30 minutes and reperfusion for 90 minutes. Observed changes in arrhythmia score, myocardial infarct size, myocardial superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA), etc. . RESULTS: Compared with the ischemia-reperfusion model group, the arrhythmia scores of the DK group and Morinda oligosaccharides 2.8g/(kg·d) and 1.4g/(kg·d) administration group were significantly reduced, and myocardial infarct area was significantly increased. After being reduced, the activities of SOD, CAT and GSH-Px in myocardium were significantly increased, while the content of MDA was significantly decreased (P<0.01). Conclusion: Morinda officinalis has protective effect on myocardium and anti-myocardial ischemia-reperfusion injury, and its mechanism is mainly related to the improvement of myocardial anti-chloride enzyme activity and reduction of lipid peroxidation.