| 崔华楠 周自强 王妍军 吴明营.氧化苦参碱预处理对急性心肌梗死大鼠的保护作用与机制[J].现代生物医学进展英文版,2014,14(33):6411-6414. |
| 氧化苦参碱预处理对急性心肌梗死大鼠的保护作用与机制 |
| Protective Effects and Mechanisms of Oxymatrine Pretreatment on a RatModel of Acute Myocardial Infarction |
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| DOI： |
| 中文关键词: 氧化苦参碱 心肌梗死 凋亡 炎症反应 氧化应激 |
| 英文关键词: Oxymatrine Myocardial infarction Apoptosis Inflammatory response Oxidative stress |
| 基金项目:北京市教委科技发展计划项目（KM201010025018） |
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| 中文摘要: |
| 目的：探讨氧化苦参碱(OMT)对冠脉结扎诱导的急性心肌梗死大鼠的保护作用与机制。方法：将SD 大鼠随机分为4 组：假
手术组、假手术+OMT 组、心梗模型组，OMT 预处理组(ig 给予OMT 100 mg/kg)。给药12 小时后，结扎冠状动脉左前降支(LAD)
复制大鼠急性心肌梗死模型。8 小时后，取大鼠心肌组织，通过TUNEL 染色观察大鼠心肌细胞损伤及凋亡情况；收集大鼠血清，
检测LDH与CK水平，过氧化氢酶(CAT)、超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH)的活力，丙二醛(MDA)含量，ELISA
法分析血清中IL-1beta、IL-6 和TNF-alpha的水平。结果：与假手术组比较，模型组大鼠的凋亡心肌细胞数明显增加(P<0.05)，血清CK、
LDH 水平显著升高(P<0.05)；同时，血清CAT、SOD与GSH 的活性明显降低(P<0.001)，MDA的含量、IL-1beta、IL-6 和TNF-alpha水平显
著增加(P<0.001)。OMT预处理明显减轻了心肌梗死大鼠心肌细胞的损伤和凋亡，降低了其血清MDA含量，IL-1beta、IL-6 和TNF-alpha
水平，增加了其CAT、SOD与GSH的活性。结论：氧化苦参碱预处理能够显著减轻心肌梗死大鼠的心肌损伤，这可能与其抗炎、抗
凋亡与抗氧化损伤作用有关。 |
| 英文摘要: |
| Objective:To explore the protective effects and mechanisms of oxymatrine pretreatment on coronary artery ligation
induced myocardial infarction.Methods:SD rats were randomly assigned into sham, sham+OMT, myocardial infarction, and OMT
pretreatment groups. OMT (100 mg/kg) was given orally before the left anterior descending branch of coronary artery (LAD) ligation
operation. LAD ligation induced rat myocardial infarction models of rat were made 12 hours after the administration of OMT. After 8
hours’observation, rat cardiac tissue was obtained and TUNEL staining was performed to analyze the injury and apoptosis of myocardial
cells. Rat serum was collected, and LDH, CK, activities of CAT, SOD, GSH, and MDA levels were detected. Inflammatory factors of
IL-1beta, IL-6, and TNF-alpha were detected by ELISA.Results:Compared with the sham group, the LAD ligation myocardial infarction
resulted in significant injuries and myocardial cells apoptosis. Significantly increased levels of CK, LDH, inflammatory factors, and
MDA; and obviously decreased CAT, SOD, and GSH were found after myocardial infarction. OMT pretreatment attenuated myocardial
infarction induced injuries and apoptosis of rat myocardial cells; decreased inflammatory factors expression and MDA production,
increased levels of CAT, SOD, and GSH.Conclusion:OMT pretreatment attenuated myocardial infarction induced cardiac injuries; and
the underlying mechanisms may due to its anti-inflammation, anti-apoptosis, and anti-oxidative effects. |
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