本文選題：缺血再灌注　切入點(diǎn)：肢體缺血后處理　出處：《桂林醫(yī)學(xué)院》2014年碩士論文　論文類型：學(xué)位論文

【摘要】：目的：探討p38MAPK信號(hào)轉(zhuǎn)導(dǎo)通路在肢體缺血后處理減輕大鼠腦缺血再灌注損傷中的作用。方法：將大鼠隨機(jī)分為假手術(shù)組(sham組)、缺血再灌注組(I/R組)、肢體缺血后處理組(LPostC組)、肢體缺血后處理+p38MAPK抑制劑SB203580組(LPostC+SB組)，線栓法建立局灶性腦缺血再灌注模型，采用雙側(cè)下肢股動(dòng)脈夾閉10min、開放10min三個(gè)循環(huán)模型。缺血2h再灌注24h，進(jìn)行神經(jīng)功能缺損評(píng)分，HE染色觀察腦組織病理形態(tài)學(xué)改變，用TUNEL法檢測(cè)神經(jīng)細(xì)胞凋亡，用免疫組化法觀察腦組織磷酸化ATF-2表達(dá)，western blot檢測(cè)大鼠額頂部腦皮質(zhì)磷酸化p38MAPK蛋白含量。結(jié)果：（1）與sham組比較，I/R組大鼠出現(xiàn)明顯神經(jīng)功能缺損及腦組織缺血改變；與I/R組比較，LPostC組、LPostC+SB組神經(jīng)功能缺損、腦組織缺血改變明顯減輕；與LPostC組比較，LPostC+SB組腦組織缺血改變減輕。（2）與sham組比較，I/R組額頂部皮質(zhì)凋亡細(xì)胞數(shù)明顯增加；與I/R組比較，LPostC組、LPostC+SB組凋亡細(xì)胞顯著減少；與LPostC組比較，LPostC+SB組凋亡細(xì)胞減少（均P0.05）。（3）與sham組比較，I/R組額頂部皮質(zhì)磷酸化p38MAPK及磷酸化ATF-2表達(dá)明顯增加；與I/R組比較，LPostC組、LPostC+SB組磷酸化p38MAPK及磷酸化ATF-2表達(dá)均顯著減少；與LPostC組比較，LPostC+SB組磷酸化p38MAPK及磷酸化ATF-2表達(dá)明顯減少（均P0.05）。結(jié)論：肢體缺血后處理對(duì)腦缺血再灌注損傷具有保護(hù)作用，，其機(jī)制可能與抑制p38MAPK激活，降低磷酸化ATF-2蛋白表達(dá)，從而抑制細(xì)胞凋亡有關(guān)。
[Abstract]:Objective: to investigate the role of p38MAPK signal transduction pathway in reducing cerebral ischemia-reperfusion injury in rats after limb ischemia. Methods: rats were randomly divided into sham group, ischemia reperfusion group and I / R group. The model of focal cerebral ischemia-reperfusion was established in the LPostC group, the limb ischemic p38MAPK inhibitor SB203580 group, and the LPostC SB group, the focal cerebral ischemia-reperfusion model was established by the method of thread embolization. The femoral arteries of the lower extremities were clamped for 10 minutes and the three circulatory models of 10min were opened. After 2 hours of ischemia and 24 hours of reperfusion, the pathological changes of brain tissue were observed by HE staining and the apoptosis of nerve cells was detected by TUNEL method. The expression of phosphorylated ATF-2 in brain tissue was detected by Western blot method. Results compared with sham group, there were obvious neurological deficits and cerebral ischemia changes in sham group. Compared with the I / R group, the neurological impairment and cerebral ischemia in LPostC SB group were significantly alleviated, and those in LPostC SB group were alleviated compared with that in LPostC group. (2) compared with sham group, the number of apoptotic cells in the parietal cortex of the I / R group was significantly higher than that in the sham group. Compared with the I / R group, the apoptotic cells in LPostC SB group were significantly decreased, and the expression of phosphorylated p38MAPK and phosphorylated ATF-2 in the frontal parietal cortex were significantly increased in the LPostC SB group compared with the sham group (P 0.05, P 0.05, P < 0.05), and the expression of phosphorylated ATF-2 in the frontal parietal cortex of the sham group was significantly higher than that in the sham group. Compared with I / R group, the expression of phosphorylated p38MAPK and phosphorylated ATF-2 decreased significantly in LPostC group. Compared with LPostC group, the expression of phosphorylated p38MAPK and phosphorylated ATF-2 in LPostC SB group was significantly decreased (P 0.05). Conclusion: limb ischemic post-treatment has protective effect on cerebral ischemia-reperfusion injury, which may be related to inhibition of p38MAPK activation and decrease of phosphorylated ATF-2 protein expression. It is related to inhibition of apoptosis.
【學(xué)位授予單位】：桂林醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類號(hào)】：R743.3


本文編號(hào)：1648153