本文選題：右美托咪定　切入點(diǎn)：腸缺血再灌注　出處：《西南醫(yī)科大學(xué)》2017年碩士論文

【摘要】：目的:研究右美托咪定(dexmedetomidine)對(duì)大鼠腸缺血再灌注所致(I/R)肝損傷的保護(hù)作用及其機(jī)制。方法:清潔級(jí)成年健康雄性Dawley-Sprague(SD)大鼠,隨機(jī)分為4組:假手術(shù)組(Sham組)、缺血再灌注組(I/R組)、2.5ug/(kg/h)右美托咪定預(yù)處理缺血再灌注組(I/R+DL組)和5ug/(kg/h)右美托咪定預(yù)處理缺血再灌注組(I/R+DH組),其中Sham組僅分離腸系膜上動(dòng)脈(SMA)而不夾閉,開(kāi)腹90min后關(guān)閉腹腔;I/R和右美托咪定處理組采用夾閉SMA 90 min后再灌注的方法制備腸缺血再灌注模型。I/R+DL組和I/R+DH組手術(shù)前1h給予尾靜脈輸注右美托咪定2.5ug/(kg/h)和5ug/(kg/h);I/R組,手術(shù)前1小時(shí)給尾靜脈輸注等量的生理鹽水。在實(shí)施再灌注2小時(shí)后,在各組隨機(jī)抽取8只大鼠,采集肝組織并利用蘇木素-伊紅染色處理,放置在顯微鏡下觀(guān)察肝臟病理結(jié)構(gòu)變化;采用Western bloting檢測(cè)促凋亡蛋白cleaved caspase 3的表達(dá)水平。并利用原位末端脫氧核苷酸轉(zhuǎn)移酶介導(dǎo)的d UTP缺口末端標(biāo)記法(TUNEL法)檢測(cè)肝細(xì)胞凋亡,然后計(jì)算出相應(yīng)的細(xì)胞凋亡指數(shù)。測(cè)定血清丙氨酸氨基轉(zhuǎn)移酶(alanine Aminotrans ferase,ALT)、門(mén)冬氨酸氨基轉(zhuǎn)移酶(Aspartate aminotrans ferase,AST)、乳酸脫氫酶(LDH)白細(xì)胞介素-6(IL-6)和腫瘤壞死因子-α(TNF-α)水平;同時(shí)檢測(cè)肝臟活性氧(ROS)、丙二醛(MDA)、超氧化物歧化酶(SOD)及髓過(guò)氧化物酶(MPO)活性。結(jié)果:與Sham組比較,I/R組、DL組及DH組大鼠肝損傷明顯,caspase-3蛋白表達(dá)量、凋亡指數(shù)、ROS、MDA、IL-6、TNF-α及MPO含量明顯增加,而SOD活性減少,差異有統(tǒng)計(jì)學(xué)意義(P0.05或0.01)。與I/R組比較,DL組及DH組以上指標(biāo)得到明顯改善,差異有統(tǒng)計(jì)學(xué)意義(P0.05或0.01);與DL組比較,DH組以上指標(biāo)得到一定程度改善,差異有統(tǒng)計(jì)學(xué)意義(P0.05或0.01)。結(jié)論:1、腸缺血再灌注可以誘發(fā)遠(yuǎn)隔器官肝臟損傷。2、右美托咪定對(duì)大鼠腸缺血再灌注所致肝損傷具有保護(hù)作用,這種保護(hù)效應(yīng)可能具有劑量依賴(lài)性。3、其機(jī)制可能與一定程度上抑制炎性反應(yīng)、氧化應(yīng)激損傷及肝細(xì)胞凋亡有關(guān)。
[Abstract]:Aim: to study the protective effect of dexmemedetomidine on hepatic injury induced by intestinal ischemia and reperfusion in rats and its mechanism. They were randomly divided into four groups: sham group (sham group), ischemia reperfusion group (I / R group) 2.5 ugr / kg / h) right metoimidine preconditioning ischemia reperfusion group (I / R DL group) and dexmetomidine preconditioning ischemia reperfusion group (I / R DH group), in which only intestinal system was isolated in Sham group. Superior membranous artery (SMA) without clipping, After opening 90min, I / R and dexmetomidine treatment group were used to make intestinal ischemia reperfusion model by clamping up SMA 90 min and reperfusion. Ir / R DL group and I / R DH group were given caudal vein infusion of dexmetomidine 2.5 ugr / kg / kg 路h / h before operation, and 5 ugr / kg / kg / h / I / R group, respectively. After 2 hours of reperfusion, 8 rats were randomly selected in each group. Liver tissues were collected and treated with hematoxylin-eosin staining. The expression of apoptotic protein cleaved caspase 3 was detected by Western bloting, and the apoptosis of hepatocytes was detected by in situ terminal deoxynucleotidyl transferase-mediated d UTP Nick end labeling (Tunel). Then the corresponding apoptotic index was calculated and the levels of serum alanine Aminotrans ferase (alt), aspartate aminotrans transferase (AST) and tumor necrosis factor- 偽 (TNF- 偽) were measured. The activity of reactive oxygen species (Ros), malondialdehyde (MDA) MDAA, superoxide dismutase (SOD) and myeloperoxidase (MPO) were also detected. Results: compared with Sham group, the expression of caspase-3 protein and the content of TNF- 偽 and MPO were significantly increased in DL-dl group and DH group. Compared with I / R group, the above indexes of DL group and DH group were obviously improved, the difference was statistically significant (P0.05 or 0.01), and the above indexes of DH group were improved to some extent compared with DL group. Conclusion the intestinal ischemia-reperfusion can induce liver injury of distant organs. Dexmetomidine has protective effect on hepatic injury induced by intestinal ischemia-reperfusion in rats. The protective effect may be dose-dependent, and its mechanism may be related to the inhibition of inflammatory response, oxidative stress injury and hepatocyte apoptosis to some extent.
【學(xué)位授予單位】：西南醫(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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