返回 
加入收藏
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
x
请在关注微信后，向客服人员索取文件
| 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 |
| TITLE： | |
| 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 |
| 阅读数： | 259 次 |
| 本月下载数： | 3 次 |
* 注：未经本站明确许可，任何网站不得非法盗链资源下载连接及抄袭本站原创内容资源!在此感谢您的支持与合作！
