重癥急性胰腺炎大鼠DDFA對(duì)肺損傷細(xì)胞凋亡及Bax, Bcl

作者：史學(xué)深，方馳華，朱明德，何鄒駿，陳鐵軍

【關(guān)鍵詞】 危重病；急性��；胰腺炎；肺/損傷；細(xì)胞凋亡；DDFA
【Abstract】　AIM: To explore the effects of DDFA on cell apoptosis and expressions of Bax and Bcl2 in lung tissue of rats with severe acute pancreatitis(SAP). METHODS: 45 rats weighting 200250 g were randomized into 3 groups: control group (n=15), SAP group (n=15) and DDFA group (n=15). The models of SAP were established by the injection of 200 g/L arginine solution ip（once a hour for 2 h） into the rats. At the 24, 48 and 72 h after establishment of models, serum amylase, TNFa and calcium were determined. The left lungs were taken for light and electron microscopic observation. Cell apoptosis in lung tissue was determined by TUNEL method. Expressions of Bax and Bcl2 were detected by immunohistochemical staining of SABC. RESULTS: In the SAP group, serum amylase, TNFa, apoptotic index, expressions of Bax and Bcl2 markedly increased. Lung tissue injuries were significant under a light microscope. As compared with SAP group at the same phase, serum amylase, TNFa, apoptotic index and expressions of Bax in DDFA group decreased significantly. While the expression of Bcl2 increased significantly. The injury of lung tissue was relieved by DDFA. CONCLUSION: The apoptosis and the expressions of Bax and Bcl2 in lung tissue might be involved in pathogenesis of SAP. DDFA administration in the early stage is helpful for diminishing lung injury induced by SAP.
【Keywords】　critical illness; acute disease; pancreatitis; lung/injuries; apoptosis; DDFA
【摘要】　目的： 探討DDFA對(duì)重癥急性胰腺炎(SAP)大鼠肺組織內(nèi)細(xì)胞凋亡及Bax,Bcl2基因表達(dá)的影響. 方法： 大鼠45只隨機(jī)分為對(duì)照組（CG）， SAP組和DDFA治療組，每組15只. 大鼠SAP模型采用分2次ip 200 g/L精氨酸溶液方法建立，建模后24, 48和72 h時(shí)測定血清TNFa，淀粉酶. 血鈣及光鏡觀察肺組織病理變化，細(xì)胞凋亡原位檢測(TUNEL)法測定肺組織內(nèi)細(xì)胞凋亡，SABC免疫組化染色法測定肺組織Bax, Bcl2基因表達(dá). 結(jié)果： SAP組血清淀粉酶, TNFa和肺組織內(nèi)細(xì)胞凋亡指數(shù), Bax, Bcl2基因表達(dá)較CG組升高，光鏡下見肺組織損害明顯；經(jīng)DDFA治療后，血清淀粉酶, TNFa和肺組織內(nèi)細(xì)胞凋亡指數(shù), Bax基因表達(dá)下降，而Bcl2基因表達(dá)增強(qiáng)，光鏡下見肺組織損害減輕. 結(jié)論： 肺組織細(xì)胞凋亡, Bax, Bcl2基因表達(dá)參與SAP發(fā)病機(jī)制，在SAP早期給予DDFA治療對(duì)減輕肺臟損害是有益的.
【關(guān)鍵詞】　危重��；急性�。灰认傺�；肺/損傷；細(xì)胞凋亡；DDFA
0引言
重癥急性胰腺炎(severe acute pancreatitis, SAP)常并發(fā)多器官功能障礙，其胰外器官損傷中肺損傷最為常見，稱之為： 急性胰腺炎相關(guān)性肺損傷［1］，其發(fā)病機(jī)制尚不完全清楚. 1997年方馳華等［2］應(yīng)用DDFA方案(D： dexamethasone； D： dextran； F： 5Fluorouracil； A： Appotininum)治療SAP取得明顯效果. 我們利用SAP肺臟損害大鼠模型，探討細(xì)胞凋亡和Bax, Bcl2基因表達(dá)在SAP肺臟損害發(fā)病機(jī)制中的作用以及應(yīng)用DDFA治療后的影響.
1材料和方法
1.1材料SD大鼠45只，雌雄不限，體質(zhì)量2

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