山核桃叶总黄酮对小鼠抗心肌缺血及心肌细胞缺氧损伤保护作用研究
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浙江中医药大学,浙江 杭州 310053

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R285.5

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* 基金项目: 国家自然科学基金(81303258);浙江省医药卫生科技计划项目(Y201233485);中国博士后科学基金 (2014M550335) 收稿日期: 2015 - 06 - 02 作者简介: 慈海登(1986-),男,河北阜城人,在读硕士研究生,研究方向:中医药抗感染与免疫调节作用的研究。△通信作者:丁志山,E-mail:zjtcmdzs@163.com


The Mechanisms of the Total Flavonoid in Hickory Leaves on Anti-myocardial Ischemia in Miceand the Protective Study of Hypoxia Injury of Myocardial Cells
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Zhejiang Chinese Medical Univesity, Hangzhou 310053, China

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    摘要:

    目的探究山核桃叶总黄酮对小鼠心肌缺血及心肌细胞(H9c2)缺氧损伤的保护作用及机制。方法1. 建立皮下注射盐酸异丙肾上腺素造成小鼠急性心肌缺血模型,心脏切片HE染色,并测定小鼠血清中肌酸激酶(CK)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、丙二醛(MDA)含量。2. 建立心肌细胞过氧化氢缺氧损伤模型,观察细胞形态,测定细胞存活率并检测细胞培养液中CK、SOD、MDA含量。结果与模型组相比,山核桃叶总黄酮高中低剂量组的心肌组织完整,炎症因子较少,血清中CK、LDH、MDA的活性显著降低,SOD活性显著升高;山核桃叶总黄酮各剂量组均能显著提高过氧化氢损伤心肌细胞的存活率,抑制LDH的释放,减少MDA的生成,提高SOD活性。结论山核桃叶总黄酮对小鼠心肌缺血及心肌细胞缺氧损伤具有保护作用。

    Abstract:

    Objective To investigate the mechanisms of total Flavonoid in Hickory Leaves on anti-myocardial ischemia in mice and the protective study of hypoxia injury of myocardial cells(H9c2). Methods 1. Establish the model in mice.subcutaneous injection of hydrochloric acid isopropyl adrenaline cause acute myocardial ischemia; hearts slicing; HE staining; and determine contents of the Creatine Kinase(CK)、 lactate dehydrogenase(LDH)、 Superoxide Dismutase(SOD)、 Malondialdehyde(MDA) in mice serums. 2. Establish the model of hypoxia injury of myocardial cells injury by H2O2; observe cells morphology; determine cells survival rate and contents of the Creatine Kinase(CK)、 Superoxide Dismutase(SOD)、 Malondialdehyde(MDA) in the cells culture medium. Results Compared with the model group, total flavonoid could decrease inflammatory cytokines in the myocardial tissue, could effectively decrease serums LDH、 MDA and CK enzymic activity, increase the level of SOD. The total flavonoid could significantly increased the viability of myocardial cells, inhibited the release of LDH, decreased the content of MDA, increased SOD activity. Conclusion The total flavonoid in hickory Leaves has protective effects on myocardial ischemia in mice and hypoxia injury of myocardial cells.

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