| 赵洋,李艳.阿托伐他汀对心肌梗死大鼠心肌损伤的保护作用及机制[J].安徽医药,2016,20(2):240-243. |
| 阿托伐他汀对心肌梗死大鼠心肌损伤的保护作用及机制 |
| The protective effect and mechanism of Atorvastatin on acute myocardial infarction |
| 投稿时间：2015-09-02 |
| DOI： |
| 中文关键词: 阿托伐他汀 心肌梗死 凋亡 XIAP 炎性 |
| 英文关键词: Atorvastatin myocardial infarction apoptosis XIAP inflammation |
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| 中文摘要: |
| 目的 研究阿托伐他汀对于心肌梗死大鼠心肌损伤的保护作用及机制。方法 选取SD 大鼠,通过结扎左冠状动脉前降支(LAD)建立急性心肌梗死大鼠模型。选取造模成功后大鼠24 只,随机分为假手术组,模型组和阿托伐他汀组,每组8只。造模观察24 h后,阿托伐他汀按照8 mg·kg-1剂量灌胃给药,模型组、假手术组均采用等量生理盐水灌胃给药,每天1次。3周后处死大鼠,取心肌并分离血清。TUNEL法检测心肌细胞凋亡；ELISA检测血清CK、TNF-α、IL-10及IL-6的含量；Western检测凋亡相关蛋白bcl-2、bax、caspase9/3、cyto C 以及 XIAP的表达变化。结果 与假手术组比较,模型组心肌凋亡率显著上升,CK、TNF-α、IL-10及IL-6含量升高,cyto C、bax 以及caspase蛋白的表达显著提升,而 bcl-2 和 XIAP 的表达则显著降低；阿托伐他汀降低了心肌凋亡率和血清中CK、TNF-α、IL-6的含量,提高了IL-10的含量,抑制bax、cyto C 和caspase表达,bcl-2和XIAP的表达升高。结论 阿托伐他汀对心肌梗死模型大鼠心肌损伤具有保护作用,其机制可能与减少氧化应激的产生,改变线粒体膜的通透性,影响凋亡相关蛋白XIAP等的表达以及改变炎性因子的释放有关。 |
| 英文摘要: |
| Objective To explore the protective effect and mechanism of Atorvastatin on acute myocardial infarction.Methods Established the model of myocardial infarction (AMI) via ligation of the left anterior descending branch in 24 rats.Divided these rats randomly into 3 groups,i.e.sham group,AMI group and Atorvastatin treatment group.Rats in sham group and AMI group were treated with normal saline while with Atorvastatin (8 mg·kg-1)in Atorvastatin treatment group.After three weeks,these rats were sacrificed,and the myocardium tissue and serum were isolated.Myocardium apoptosis was detected by TUNEL assay,the amounts of CK,TNF-α,IL-10 and IL-6 were evaluated with ELISA kit and the expression of bcl-2,bax,cyto-c,caspase3/9 and XIAP were detected by western blot.Results The amounts of CK,TNF-α,IL-6,IL-10 and apoptosis rate were increased in AMI group.The expressions of cytoC,bax,caspase3/9 were elevated in AMI rgoup,while the expressions of bcl-2 and XIAP were down-regulated.Atorvastatin significantly decreased the amounts of CK,TNF-α,IL-6,and the apoptosis rate,and increased the amount of IL-10.It also down-regulated the expressions of cytoC,bax,caspase3/9 and up-regulated the expressions of bcl-2 and XIAP. Conclusions Atorvastatin can protect the myocardium in acute myocardial infarction from apoptosis by decreasing the oxidative stress and the open of mitochondrial permeability transition pore (PTP),regulating the expressions of apoptosis relative proteins bcl-2,bax,caspase9/3,cytoC and XIAP,and inhibiting the inflammation response. |
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