【摘要】：目的:通過復(fù)制1型糖尿病大鼠的腦缺血再灌動物模型,觀察七氟醚后處理對糖尿病大鼠局灶性腦缺血再灌注損傷后STAT3信號通路的影響,并探討其作用機制。方法:成年SD雄性大鼠適應(yīng)性飼養(yǎng)及空腹12h后,腹腔注射鏈脲佐菌素(STZ)60mg/kg制備T1DM模型。按隨機分組原則分為4組:假手術(shù)(Sham)組、缺血再灌注(IR)組、七氟醚后處理(Sevo)組、阻斷劑(B)組,每組各10只。參照Zea Longa線栓法制備大鼠局灶性腦缺血再灌注模型,采用Longa評分法進行神經(jīng)行為學(xué)評分,HE染色觀察組織結(jié)構(gòu)的病理變化,ELISA檢測血清s-100β蛋白含量,Western blot檢測stat3、p-stat3的表達情況,以及對腦梗面積進行測量。結(jié)果:與Sham組相比,IR組的神經(jīng)行為學(xué)評分、梗死面積及血清s-100β蛋白含量明顯升高(P0.01);與IR組相比,Sevo組及B組的神經(jīng)行為學(xué)評分、梗死面積及血清s-100β蛋白含量明顯降低(P0.05);Sevo組與B組比較各指標(biāo)均無明顯差異。在Stat3總蛋白表達量上,各組間差異無統(tǒng)計學(xué)意義(P0.05);而在磷酸化Stat3的表達方面與Stat3總蛋白類似,Sevo組與IR組的磷酸化Stat3表達量差異無統(tǒng)計學(xué)意義(P0.05)。與其余各組相比,B組磷酸化Stat3表達量明顯下降,(P0.05)。結(jié)論:在1型糖尿病模型大鼠中,七氟醚后處理對缺血再灌注腦組織是有保護作用的,但這短期(24h)保護作用并非通過Stat3信號傳導(dǎo)通路活化來完成的。
[Abstract]:Aim: to investigate the effect of sevoflurane post-treatment on STAT3 signal pathway after focal cerebral ischemia-reperfusion injury in type 1 diabetic rats. Methods: adult SD male rats were fed with streptozotocin (STZ) 60mg/kg) for 12 hours on an empty stomach. T1DM model was established by intraperitoneal injection of streptozotocin (STZ) 60mg/kg). According to the principle of random grouping, they were divided into 4 groups: sham operation (Sham) group, ischemia reperfusion (IR) group, sevoflurane post-treated (Sevo) group, and blocker (B) group, 10 rats in each group. The rat model of focal cerebral ischemia-reperfusion was established by Zea Longa thread embolization method. The neurobehavioral score was evaluated by Longa scoring method, the pathological changes of tissue structure were observed by HE staining, and the serum s-100 尾 protein content by ELISA was detected by, Western blot to detect stat3,. The expression of p-stat3 and the area of cerebral infarction were measured. Results: compared with Sham group, the neurobehavioral score, infarct size and serum s-100 尾 protein content in IR group were significantly increased (P0.01). Compared with IR group, the neurobehavioral score, infarct size and serum s-100 尾 protein content in Sevo and B groups were significantly lower than those in IR group (P0.05). There was no significant difference in each index between); Sevo group and B group. In the total protein expression of Stat3, there was no significant difference among the groups (P0.05), but the expression of phosphorylated Stat3 was similar to the total protein of Stat3. There was no significant difference in the expression of phosphorylated Stat3 between Sevo group and IR group (P0.05). Compared with other groups, the expression of phosphorylated Stat3 in group B was significantly decreased (P0.05). Conclusion: sevoflurane post-treatment has protective effect on cerebral ischemia-reperfusion in type 1 diabetic rats, but the short-term (24h) protective effect is not achieved by activation of Stat3 signal transduction pathway.
【學(xué)位授予單位】：暨南大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：R614

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