重症急性胰腺炎大鼠DDFA对肺损伤细胞凋亡及Bax, Bcl_医学论文.docVIP

重症急性胰腺炎大鼠DDFA对肺损伤细胞凋亡及Bax, Bcl_医学论文.doc

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重症急性胰腺炎大鼠DDFA对肺损伤细胞凋亡及Bax, Bcl_医学论文.doc

重症急性胰腺炎大鼠DDFA对肺损伤细胞凋亡及Bax, Bcl_医学论文 重症急性胰腺炎大鼠DDFA对肺损伤细胞凋亡及Bax, Bcl_医学论文 作者:史学深,方驰华,朱明德,何邹骏,陈铁军 【关键词】 危重病;急性病;胰腺炎;肺/损伤;细胞凋亡;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: 探讨DDFA对重症急性胰腺炎(SAP)大鼠肺组织内细胞凋亡及Bax,Bcl2基因表达的影响. 方法: 大鼠45只随机分为对照组(CG), SAP组和DDFA治疗组,每组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时测定血清TNFa,淀粉酶. 血钙及光镜观察肺组织病理变化,细胞凋亡原位检测(TUNEL)法测定肺组织内细胞凋亡,SABC免疫组化染色法测定肺组织Bax, Bcl2基因表达. 结果: SAP组血清淀粉酶, TNFa和肺组织内细胞凋亡指数, Bax, Bcl2基因表达较CG组升高,光镜下见肺组织损害明显;经DDFA治疗后,血清淀粉酶, TNFa和肺组织内细胞凋亡指数, Bax基因表达下降,而Bcl2基因表达增强,光镜下见肺组织损害减轻. 结论: 肺组织细胞凋亡, Bax, Bcl2基因表达参与SAP发病机制,在SAP早期给予DDFA治疗对减轻肺脏损

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