辛伐他汀对老年小鼠心肌缺血再灌注时氧化应激及细胞凋亡的影响
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篇名: 辛伐他汀对老年小鼠心肌缺血再灌注时氧化应激及细胞凋亡的影响
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摘要: 目的:研究辛伐他汀对老年小鼠心肌缺血再灌注(IR)时氧化应激及细胞凋亡的影响。方法:取老年小鼠随机分为假手术组(磷酸盐缓冲液)、模型组(磷酸盐缓冲液)和辛伐他汀低、中、高剂量组(2.5、5、20 mg/kg),每组14只。各组小鼠于造模前ip相应药物7 d,每天1次。除假手术组外其余各组小鼠复制IR模型。检测各组小鼠心肌梗死面积比例、心肌细胞凋亡率、心肌组织中凋亡基因Caspase-3活性、Bax和Bcl-2蛋白表达、蛋白激酶B(Akt)磷酸化水平、血清中丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性。结果:与假手术组比较,模型组小鼠心肌梗死面积比例、心肌细胞凋亡率、Caspase-3活性、Bax蛋白表达和MDA含量均增加,Bcl-2蛋白表达、Akt磷酸化水平和SOD活性均降低(P<0.01);与模型组比较,辛伐他汀高剂量组小鼠心肌梗死面积比例、心肌细胞凋亡率、Caspase-3活性、Bax蛋白表达、MDA含量均降低,Bcl-2蛋白表达、Akt磷酸化水平、SOD活性均升高(P<0.01);辛伐他汀低、中剂量组小鼠上述指标差异均无统计学意义(P>0.05)。结论:辛伐他汀能显著减轻老年小鼠心肌IR损伤,其机制可能与抑制心肌细胞凋亡和氧化应激产物生成有关。
ABSTRACT: OBJECTIVE: To study the effects of simvastatin on oxidative stress and cell apoptosis in aged mice with myocardial ischemia-reperfusion (IR). METHODS: Aged mice were randomly divided into sham operation group (phosphate buffer solution), model group (phosphate buffer solution) and simvastatin low-dose, medium-dose and high-dose groups (2.5, 5 and 20 mg/kg) with 14 mice in each group. Those groups were given relevant medicine intraperitoneally before modeling for 7 d, once a day. IR model was induced in those groups except for sham operation group. The area ratio of myocardial infarction, myocardial cell apoptosis rate, activity of myocardial tissue apoptosis gene Caspase-3, the protein expression of Bax and Bcl-2, Akt phosphorylation, serum concent of MDA and activity of SOD were all detected. RESULTS: Compared with sham operation group, the area ratio of myocardial infarction, myocardial cell apoptosis rate, Caspase-3 activity, the protein expression of Bax and MDA content were all increased in model group, while the protein expression of Bcl-2, Akt phosphorylation and SOD activity were decreased (P<0.01). Compared with model group, the area ratio of myocardial infarction, myocardial apoptosis rate, Caspase-3 activity, the protein expression of Bax and MDA content were all decreased in simvastatin high-dose group, while the protein expression of Bcl-2, Akt phosphorylation and SOD activity were increased (P<0.01). There was no statistical significance in above indexes in simvastatin low-dose and medium-dose groups (P>0.05). CONCLUSIONS: Simvastatin can relieve myocardial IR injury in aged mice, and the mechanism of which may be associated with inhibiting myocardial cell apoptosis and the generation of oxidative stress.
期刊: 2016年第27卷第19期
作者: 廖小龙,王首红,王中华,郭伟新,温剑艺,覃铁和
AUTHORS: LIAO Xiaolong,WANG Shouhong,WANG Zhonghua,GUO Weixin,WEN Jianyi,QIN Tiehe
关键字: 辛伐他汀;心肌缺血再灌注;氧化应激;心肌细胞凋亡;老年小鼠
KEYWORDS: Simvastatin; Myocardial ischemia-reperfusion; Oxidative stress; Myocardial cell apoptosis; Aged mice
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