过氧化物酶体增殖物激活受体-γ参与七氟醚后处理心肌保护作用机制的研究
发布时间:2018-07-13 20:52
【摘要】:目的:观察七氟醚对缺血再灌注心肌中PPAR-γ的影响并探讨PPAR-γ在七氟醚后处理减轻心肌缺血再灌注损伤中的作用。方法:雄性C57BL/6小鼠按随机数字表法分为4组(n=5):对照组(Control组)、七氟醚后处理组(SPostC组)、七氟醚后处理+PPAR-γ抑制剂组(SPostC+GW9662组)和PPAR-γ抑制剂组(GW9662组),各组均建立小鼠在体心肌缺血再灌注损伤模型(缺血30min,再灌注120min),再灌注开始15min内吸入3.4%七氟醚作为七氟醚后处理,各组均在缺血前30min腹腔注射抑制剂或安慰剂。实验中测定小鼠心肌缺血前和再灌注后的心率(HR)及平均动脉压(MAP);实验结束后留取心脏,测定心肌梗死面积及再灌注早期(30min)和再灌注晚期(120min)的心肌PPAR-γ转录活性。结果:与Control组比较,SPostC组的心肌梗死面积显著降低(P0.05),同时PPAR-γ转录活性升高(P0.05),且SPostC组再灌注120min时的PPAR-γ转录活性要高于再灌注30min时的PPAR-γ转录活性。SPostC+GW9662组、GW9662组的心肌梗死面积和PPAR-γ转录活性与Control组相比差异无统计学意义(P0.05),HR和MAP在各组各时点之间差异亦无统计学意义(P0.05)。结论:七氟醚后处理能够活化再灌注心肌中的PPAR-γ,提高其转录活性,从而降低心肌缺血再灌注损伤后的心肌梗死面积,发挥其心肌保护作用。
[Abstract]:Aim: to observe the effect of sevoflurane on PPAR- 纬 in ischemic reperfusion myocardium and to explore the role of PPAR- 纬 in reducing myocardial ischemia-reperfusion injury after sevoflurane treatment. Methods: male C57BL / 6 mice were randomly divided into four groups: control group (control group), sevoflurane post-treatment group (SPostC group), sevoflurane post-treated PPAR- 纬 inhibitor group (SPostC GW9662 group) and PPAR- 纬 inhibitor group (GW9662 group). Myocardial ischemia reperfusion injury model (ischemia 30 minutes, reperfusion 120min), reperfusion began to 15min inhalation of 3. 4% sevoflurane as sevoflurane post-treatment, 30min was intraperitoneally injected with inhibitor or placebo in each group before ischemia. Heart rate (HR) and mean arterial pressure (map) were measured before and after myocardial ischemia in mice, and myocardial PPAR- 纬 transcriptional activity in early reperfusion (30min) and late reperfusion (120min) were measured. Results: compared with control group, myocardial infarction size in SPostC group was significantly lower (P0.05), while PPAR- 纬 transcriptional activity was increased (P0.05), and the PPAR- 纬 transcriptional activity in SPostC group was higher than that in 30min reperfusion group (PPAR- 纬 transcriptional activity was higher than that in SPostC GW9662 group GW9662 group. There was no significant difference in area and PPAR- 纬 transcriptional activity between control group and control group (P0.05). Conclusion: sevoflurane post-treatment can activate PPAR- 纬 in reperfusion myocardium, increase its transcriptional activity, decrease myocardial infarction size and exert its myocardial protection.
【学位授予单位】:新疆医科大学
【学位级别】:硕士
【学位授予年份】:2017
【分类号】:R614
本文编号:2120708
[Abstract]:Aim: to observe the effect of sevoflurane on PPAR- 纬 in ischemic reperfusion myocardium and to explore the role of PPAR- 纬 in reducing myocardial ischemia-reperfusion injury after sevoflurane treatment. Methods: male C57BL / 6 mice were randomly divided into four groups: control group (control group), sevoflurane post-treatment group (SPostC group), sevoflurane post-treated PPAR- 纬 inhibitor group (SPostC GW9662 group) and PPAR- 纬 inhibitor group (GW9662 group). Myocardial ischemia reperfusion injury model (ischemia 30 minutes, reperfusion 120min), reperfusion began to 15min inhalation of 3. 4% sevoflurane as sevoflurane post-treatment, 30min was intraperitoneally injected with inhibitor or placebo in each group before ischemia. Heart rate (HR) and mean arterial pressure (map) were measured before and after myocardial ischemia in mice, and myocardial PPAR- 纬 transcriptional activity in early reperfusion (30min) and late reperfusion (120min) were measured. Results: compared with control group, myocardial infarction size in SPostC group was significantly lower (P0.05), while PPAR- 纬 transcriptional activity was increased (P0.05), and the PPAR- 纬 transcriptional activity in SPostC group was higher than that in 30min reperfusion group (PPAR- 纬 transcriptional activity was higher than that in SPostC GW9662 group GW9662 group. There was no significant difference in area and PPAR- 纬 transcriptional activity between control group and control group (P0.05). Conclusion: sevoflurane post-treatment can activate PPAR- 纬 in reperfusion myocardium, increase its transcriptional activity, decrease myocardial infarction size and exert its myocardial protection.
【学位授予单位】:新疆医科大学
【学位级别】:硕士
【学位授予年份】:2017
【分类号】:R614
【参考文献】
相关期刊论文 前1条
1 Chen Dong;Hui Zhou;Chong Shen;Lu-Gang Yu;Yi Ding;Yong-Hong Zhang;Zhi-Rong Guo;;Role of peroxisome proliferator-activated receptors gene polymorphisms in type 2 diabetes and metabolic syndrome[J];World Journal of Diabetes;2015年04期
,本文编号:2120708
本文链接:https://www.wllwen.com/shoufeilunwen/mpalunwen/2120708.html
最近更新
教材专著