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目的 :探讨芪丹通脉片 (QDTMT)对异丙肾上腺素(Iso)所致急性心肌缺血的防治作用 .方法 :给大鼠灌服QDTMT(2g·kg-1) 2wk ,皮下注射异丙肾上腺素 (Iso ,5mg·kg-1) ,诱导急性心肌缺血模型 ,测定心肌线粒体 (Mit)中丙二醛 (MDA)、超氧化物歧化酶 (SOD)、谷胱甘肽过氧化物酶(GXH PX)及琥珀酸脱氢酶 (SDH) .结果 :模型组线粒体中MDA含量增加 ,QDTMT组线粒体MDA含量显著低于模型组 [(8.9± 0 .6 )vs (5 .5± 0 .6 ) μmol·g-1,P <0 .0 1];线粒体中模型组SOD活性降低 ,QDTMT组SOD活性升高 ,两者相比较有显著性差异 [(6 73.2± 2 5 .2 )vs (5 36 .2± 2 0 .3)kNU·g-1,P <0 .0 1].QDTMT组GSH PX活力显著高于模型组 [(5 5 .3± 6 .0)vs (4 0 .7± 7.1)kNU·g-1,P <0 .0 1].QDTMT组线粒体中SDH活性明显升高 [(0 .0 7± 0 .0 1)vs (0 .0 5± 0 .0 1)kat·g-1,P <0 .0 1].结论 :QDTMT可通过降低心肌线粒体中MDA含量 ,增加SOD ,GSH PX及SDH活力 ,减轻氧自由基对心肌线粒体的损伤 .
Objective: To investigate the preventive and therapeutic effects of QDTMT on acute myocardial ischemia induced by isoproterenol (Iso). METHODS: Rats were given QDTMT (2g·kg-1) 2wk orally, subcutaneous injection of isoproterenol Epinephrine (Iso, 5mg·kg-1), Induction of Acute Myocardial Ischemia Model, Measurement of Malondialdehyde (MDA), Superoxide Dismutase (SOD), Glutathione Peroxidase in Myocardial Mitochondria (Mit) (GXH PX) and succinate dehydrogenase (SDH). Results: The MDA content in the mitochondria of the model group increased, and the mitochondrial MDA content in the QDTMT group was significantly lower than that of the model group [(8.9±0.6) vs (5. 5± 0 . 6) μmol·g-1, P <0.01; mitochondrial SOD activity in the model group decreased, and SOD activity in the QDTMT group increased, there was a significant difference between the two [(7,73.2±25.2) vs (5.32 ± 20.3) kNU·g-1, P <0. 01]. The GSH PX activity in the QDTMT group was significantly higher than that in the model group [(5 5 . 3 ± 6 .0) vs (4 0 The SDH activity in the mitochondria of the .7± 7.1) kNU·g-1, P <0.01) QDTMT group was significantly increased [(0.07±0.10) vs (0.05±0.0). 1) kat·g-1, P <0.01. Conclusion: QDTMT can reduce the oxygen free radicals to myocardial mitochondria by decreasing the MDA content in myocardial mitochondria and increasing the activity of SOD, GSH PX and SDH. Injury.