本文選題：重癥急性胰腺炎 + 心肌損傷　； 參考：《遼寧醫(yī)學(xué)院》2013年碩士論文

【摘要】：目的 研究大黃素（Emodin）對(duì)重癥急性胰腺炎（severe acute pancreatitis，SAP）大鼠心肌損傷的干預(yù)作用，并探討其作用機(jī)制。 方法 32只健康雄性SD（Sprague Dawley）大鼠隨機(jī)平均分為假手術(shù)組（A組），模型組（B組），大黃素治療組(C組)，大黃素加五羥基葵酸鈉（5-hydroxydecanoate,5-HD）治療組(D組)（5-HD可以特異性阻斷心肌mitoKATPC的開啟）。為采用5％�；悄懰徕c胰膽管逆行注射方法建立SAP模型。24小時(shí)后,采集標(biāo)本，用ELISA法測(cè)定各組大鼠血清肌鈣蛋白I（cardial troponin I,CTnI）、肌酸激酶同工酶（creatine kinase-MB，CK-MB）、腫瘤壞死因子-α（Tumor necrosis factor-α，TNF-α）水平，，全自動(dòng)生化分析儀測(cè)定24小時(shí)血清淀粉酶（amylase,AMY）水平，用免疫組化法檢測(cè)術(shù)后24小時(shí)各組大鼠心肌Bcl-2、Bax基因水平的表達(dá)，用TUNEL法檢測(cè)各組大鼠心肌細(xì)胞凋亡情況，光鏡下觀察各組大鼠胰腺及心肌組織的病理變化及電鏡下觀察心肌超微結(jié)構(gòu)改變。 結(jié)果 大黃素治療組大鼠血清CTnI、CK-MB水平，均低于SAP模型組，但仍高于假手術(shù)組，均有統(tǒng)計(jì)學(xué)意義（p0.05）；大黃素加5-HD治療組低于SAP模型組，高于大黃素治療組，差異均有統(tǒng)計(jì)學(xué)意義（p0.05）。血清TNF-α水平，大黃素治療組低于SAP組，SAP模型組與大黃素加5-HD治療組沒有顯著差異(p0.05)。SAP模型組大鼠血清AMY最高，其次為大黃素加5-HD治療組、大黃素治療組、假手術(shù)組（p0.05）。大黃素治療組心肌細(xì)胞Bax基因表達(dá)低于SAP模型組，高于假手術(shù)組(p0.05)。假手術(shù)組心肌細(xì)胞Bcl-2表達(dá)最高，大黃素治療組、大黃素加5-HD治療組、SAP模型組依次降低(p0.05)。SAP模型組凋亡指數(shù)（apoptotic index，AI）高于其他組，其次為大黃素加5-HD治療組、大黃素治療組、假手術(shù)組（p0.05）。大黃素治療組大鼠胰腺及心肌組織病理學(xué)、超微結(jié)構(gòu)損害較SAP組大鼠減輕，而SAP組大鼠與大黃素加5-HD治療組差別不明顯。 結(jié)論 大黃素能減輕SAP的病變程度和心肌損傷，其對(duì)心肌的保護(hù)作用有可能是通過抑制炎癥介質(zhì)的產(chǎn)生,激活心肌細(xì)胞線粒體膜ATP敏感性K+通道（Mitochondria sensitivitypotassium channel，mitoKATPC）對(duì)抗細(xì)胞凋亡而實(shí)現(xiàn)的。
[Abstract]:Purpose To study the effect of emodin on myocardial injury in rats with severe acute pancreatitis (SAP) and to explore its mechanism. Method 32 healthy male SD(Sprague Dawley rats were randomly divided into sham-operated group (group A), model group (group B), emodin treatment group (group C), emodin plus sodium pentachloroate (5-hydroxydecanoate 5-HDD) group (group D), which could specifically block the opening of myocardial mitoKATPC. In order to establish SAP model by retrograde injection of 5% sodium taurocholate into pancreatic bile duct, the serum levels of troponin (I(cardial troponin), creatine kinase isoenzyme (creatkinase-MBK), tumor necrosis factor- 偽 Tumor necrosis factor- 偽 (TNF- 偽) in serum of rats in each group were determined by ELISA method. The serum amylase (AMY) level was measured by automatic biochemical analyzer, the expression of Bcl-2Bax-Bax gene in myocardium of rats 24 hours after operation was detected by immunohistochemical method, and the apoptosis of cardiac myocytes in each group was detected by TUNEL method. The pathological changes of pancreas and myocardium were observed under light microscope and ultrastructure of myocardium were observed under electron microscope. Result The serum levels of CK-MB in emodin treatment group were lower than those in SAP model group, but still higher than those in sham operation group (P 0.05), and emodin plus 5-HD treatment group were lower than SAP model group and higher than emodin treatment group (P 0.05). The level of serum TNF- 偽 in the emodin treatment group was lower than that in the SAP group. There was no significant difference between the emodin model group and the emodin plus 5-HD group. The serum AMY level in the SAP model group was the highest, followed by emodin plus 5-HD treatment group, emodin treatment group and sham-operation group (p 0.05). The expression of Bax gene in cardiac myocytes in emodin treated group was lower than that in SAP model group and higher than that in sham operation group. The expression of Bcl-2 in cardiomyocytes of sham operation group was the highest, and that of emodin treatment group, emodin plus 5-HD treatment group and emodin plus 5-HD treatment group was significantly lower than that of other groups, followed by emodin + 5-HD treatment group, emodin treatment group and sham operation group (P 0.05). The histopathology and ultrastructure damage of pancreas and myocardium in the emodin treatment group was less than that in the SAP group, but there was no significant difference between the SAP group and the emodin plus 5-HD group. Conclusion Emodin can attenuate the pathological changes and myocardial injury of SAP. The protective effect of emodin on myocardium may be achieved by inhibiting the production of inflammatory mediators and activating Mitochondria sensitivitypotassium channel Mitochondria sensitivitypotassium channel Mitmito KATPC. it is possible that emodin can inhibit the production of inflammatory mediators and activate Mitochondria sensitivitypotassium channel mito KATPC.
【學(xué)位授予單位】：遼寧醫(yī)學(xué)院
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2013
【分類號(hào)】：R657.51

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