【摘要】：目的:觀察七氟醚對(duì)缺血再灌注心肌中PPAR-γ的影響并探討PPAR-γ在七氟醚后處理減輕心肌缺血再灌注損傷中的作用。方法:雄性C57BL/6小鼠按隨機(jī)數(shù)字表法分為4組(n=5):對(duì)照組(Control組)、七氟醚后處理組(SPostC組)、七氟醚后處理+PPAR-γ抑制劑組(SPostC+GW9662組)和PPAR-γ抑制劑組(GW9662組),各組均建立小鼠在體心肌缺血再灌注損傷模型(缺血30min,再灌注120min),再灌注開(kāi)始15min內(nèi)吸入3.4%七氟醚作為七氟醚后處理,各組均在缺血前30min腹腔注射抑制劑或安慰劑。實(shí)驗(yàn)中測(cè)定小鼠心肌缺血前和再灌注后的心率(HR)及平均動(dòng)脈壓(MAP);實(shí)驗(yàn)結(jié)束后留取心臟,測(cè)定心肌梗死面積及再灌注早期(30min)和再灌注晚期(120min)的心肌PPAR-γ轉(zhuǎn)錄活性。結(jié)果:與Control組比較,SPostC組的心肌梗死面積顯著降低(P0.05),同時(shí)PPAR-γ轉(zhuǎn)錄活性升高(P0.05),且SPostC組再灌注120min時(shí)的PPAR-γ轉(zhuǎn)錄活性要高于再灌注30min時(shí)的PPAR-γ轉(zhuǎn)錄活性。SPostC+GW9662組、GW9662組的心肌梗死面積和PPAR-γ轉(zhuǎn)錄活性與Control組相比差異無(wú)統(tǒng)計(jì)學(xué)意義(P0.05),HR和MAP在各組各時(shí)點(diǎn)之間差異亦無(wú)統(tǒng)計(jì)學(xué)意義(P0.05)。結(jié)論:七氟醚后處理能夠活化再灌注心肌中的PPAR-γ,提高其轉(zhuǎn)錄活性,從而降低心肌缺血再灌注損傷后的心肌梗死面積,發(fā)揮其心肌保護(hù)作用。
[Abstract]:Aim: to observe the effect of sevoflurane on PPAR- 緯 in ischemic reperfusion myocardium and to explore the role of PPAR- 緯 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- 緯 inhibitor group (SPostC GW9662 group) and PPAR- 緯 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- 緯 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- 緯 transcriptional activity was increased (P0.05), and the PPAR- 緯 transcriptional activity in SPostC group was higher than that in 30min reperfusion group (PPAR- 緯 transcriptional activity was higher than that in SPostC GW9662 group GW9662 group. There was no significant difference in area and PPAR- 緯 transcriptional activity between control group and control group (P0.05). Conclusion: sevoflurane post-treatment can activate PPAR- 緯 in reperfusion myocardium, increase its transcriptional activity, decrease myocardial infarction size and exert its myocardial protection.
【學(xué)位授予單位】：新疆醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：R614

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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

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