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作 者:杜恒[1] 刘明成[2] 李福安[1] 任世存[1] 马建滨[3] 张得钧[1,2]
机构地区:[1]青海大学医学院,青海西宁810001 [2]青海大学生态环境工程学院,青海西宁810016 [3]青海师范大学生命与地理学院,青海西宁810008
出 处:《青海医学院学报》2013年第3期203-206,共4页Journal of Qinghai Medical College
基 金:青海省科技厅基金项目(2011-Z-704)
摘 要:目的探讨藏药莪达夏对大鼠心肌缺血-再灌注损伤保护作用可能的分子机制。方法以结扎大鼠冠脉左前降支方法造成心肌缺血再灌注模型,再灌注40 min后采用酶联免疫方法检测大鼠心肌凋亡蛋白Bc1-2和Bax含量,并行组织形态学观察。结果心肌组织中Bc1-2的含量缺血再-灌注模型组明显低于正常对照组,莪达夏高、中、低剂量组均高于模型组;心肌组织中Bax的含量缺血再-灌注模型组明显高于正常对照组,莪达夏高、中、低剂量组均低于模型组。结论对大鼠心肌缺血-再灌注损伤保护作用可能的分子机制是莪达夏能够通过促进Bc1-2蛋白的表达、抑制Bax蛋白的表达从而抑制细胞凋亡的发生,发挥抗缺血缺氧性损伤的保护作用。Objective The article explored the possible protective mechanism in vivo of Oxytropis Falcate Bunge in cardiac muscular tissue of myocardial isehemia and reperfusion injury Rats. Methods The model of myo- cardial ischemia - reperfusion injury in rats was employed by ligating theartery of left anterior descending (LAD). After the following reperfusion for 40 minutes ,the concentration of the Bax and Bcl -2 protein in rats' myocardial tissue were tested, and histomorphology was observed. Results The results showed that the expression of Bcl -2 of myocardial tissue in ischemia - reperfusion model group were much lower than that of normal control group, test groups were higher than that of model group. The expression of Bax of myocardial tissue in ischemia - reperfusion model group were much higher than that of normal control group, test groups were lower than that of model group. Conclusion O. falcate Bunge could promote Bcl -2 protein expression and inhibit Bax protein expression to the occurrence of cell apoptosis, playing protective role for hypoxic - ischemic cardiac injury.
分 类 号:R542.2[医药卫生—心血管疾病]
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