依達(dá)拉奉和右美托咪定對體外循環(huán)大鼠的腦保護(hù)作用及機(jī)制研究
發(fā)布時(shí)間:2018-04-21 12:04
本文選題:依達(dá)拉奉 + 體外循環(huán); 參考:《江蘇大學(xué)》2017年碩士論文
【摘要】:第一部分:依達(dá)拉奉對體外循環(huán)大鼠腦損傷的保護(hù)作用目的依達(dá)拉奉是新型氧自由基清除劑,本研究擬觀察依達(dá)拉奉對體外循環(huán)(CPB)所致大鼠腦損傷的影響。方法雄性成年SD大鼠24只,體重400~450 g,隨機(jī)均分為三組(n=8/組),分別為假手術(shù)組(S組)、CPB組(C組)和依達(dá)拉奉組(E組)。S組穿刺但不進(jìn)行CPB;C組建立CPB模型;E組建立CPB模型并在預(yù)沖液中加入依達(dá)拉奉5 mg/kg。CPB結(jié)束后24 h經(jīng)股動(dòng)脈抽血檢測血清中白血病介素(interleukin-6,IL-6)、IL-10、神經(jīng)元特異性烯醇化酶(neuron specific enolase,NSE)和S-100β鈣結(jié)合蛋白的含量;取腦組織裂解勻漿,測丙二醛(Malondialdehyde,MDA)的含量和超氧化歧化酶(Superoxide dismutase,SOD)的活性。結(jié)果與S組相比,C組和E組的IL-6、IL-10、NSE、S-100β以及MDA含量明顯增高(P0.05),SOD活性明顯降低(P0.05)。與 C 組比較,E 組 IL-6、NSE、S-100β 和 MDA 含量明顯降低(P0.05),IL-10含量和SOD活性明顯升高(P0.05)。結(jié)論預(yù)沖液中加入5mg/kg依達(dá)拉奉可減輕CPB所致大鼠腦炎癥和氧化應(yīng)激反應(yīng),對CPB大鼠具有明顯的腦保護(hù)作用。第二部分:右美托咪定對體外循環(huán)大鼠神經(jīng)元凋亡的影響目的右美托咪定是高選擇性α 2受體激動(dòng)劑,本研究探討右美托咪定對心肺轉(zhuǎn)流(CPB)大鼠神經(jīng)元凋亡的影響。方法雄性SD大鼠24只隨機(jī)均分為以下三組(n=8/組):假手術(shù)組(S組)、CPB組(C組)和右美托咪定組(D組)。S組穿刺但不進(jìn)行CPB;C組建立CPB模型;D組CPB前20 min靜脈注射右美托咪定10μg/kg。CPB結(jié)束后24 h時(shí)處死大鼠,取腦組織,采用TUNEL法檢測凋亡細(xì)胞,計(jì)算凋亡指數(shù),采用免疫組化法檢測Bcl-2和Bax的表達(dá),計(jì)算Bcl-2/Bax比值。結(jié)果與S組相比,C組和D組凋亡指數(shù)明顯升高,Bcl-2和Bax表達(dá)上調(diào)及Bcl-2/Bax比值升高(P0.05);與C組相比,D組凋亡指數(shù)降低,Bcl-2表達(dá)上調(diào),Bax表達(dá)下調(diào),Bcl-2/Bax升高(P0.05)。結(jié)論預(yù)先靜脈注射右美托咪定10 μg/kg可抑制CPB大鼠神經(jīng)元凋亡,其機(jī)制可能與調(diào)節(jié)Bcl-2和Bax表達(dá)有關(guān),具有明顯的神經(jīng)保護(hù)作用。
[Abstract]:Part I: protective effects of Edaravone on brain injury in rats with cardiopulmonary bypass objective to investigate the effects of Edaravone on brain injury induced by CPB in rats. Methods Twenty-four adult male SD rats were used. Weight 400g, each group was randomly divided into three groups: sham operation group (group S) and Edaravone group (group E). Group S was punctured but no CPB model was established in group C (group E). CPB model was established in group E and Edaravone was added to the pre-flushing fluid. 5After the end of mg/kg.CPB, the contents of IL-10, neuron specific enolase neuron specific enolase (NSE) and S-100 尾 calcium-binding protein (S-100 尾 -calcium-binding protein) in serum were detected by femoral artery blood sampling. The content of malondialdehyde (malondialdehyde) and the activity of superoxide dismutase (SOD) were measured. Results compared with S group, the contents of IL-6, IL-10, NSES-100 尾 and MDA in group C and E were significantly higher than those in group S, and the activity of sod in group C and group E was significantly lower than that in group E. Compared with group C, the contents of IL-6NSES-100 尾 and MDA in E group significantly decreased the content of IL-10 and the activity of SOD increased significantly. Conclusion the addition of 5mg/kg Edaravone to the preflushing solution can reduce the inflammation and oxidative stress in the brain induced by CPB in rats, and has a significant protective effect on the brain of CPB rats. Part 2: effects of dexmetomidine on neuronal apoptosis in cardiopulmonary bypass rats objective to investigate the effect of dexmetomidine on apoptosis of cardiopulmonary bypass (CPB) neurons in rats with cardiopulmonary bypass (CPB). Methods Twenty-four male Sprague-Dawley rats were randomly divided into the following three groups: sham operation group (group S) and right metoimidine group (group D). The rats were killed 24 hours after the end of 10 渭 g/kg.CPB. The apoptotic cells were detected by TUNEL method and the apoptotic index was calculated. The expression of Bcl-2 and Bax was detected by immunohistochemical method and the ratio of Bcl-2/Bax was calculated. Results compared with group S, the apoptotic index of C group and D group were significantly increased, the expression of Bcl-2 and Bax and the ratio of Bcl-2/Bax were increased (P 0.05), and the expression of Bcl-2 / Bax was down-regulated in group C (P 0.05), and the expression of Bcl-2 / Bax was down-regulated in group C (P < 0.05). Conclusion intravenous dexmetidine 10 渭 g/kg can inhibit neuronal apoptosis in CPB rats. The mechanism may be related to regulating the expression of Bcl-2 and Bax, and has obvious neuroprotective effect.
【學(xué)位授予單位】:江蘇大學(xué)
【學(xué)位級別】:碩士
【學(xué)位授予年份】:2017
【分類號】:R654.1
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