高迁移率族蛋白-1在急性胰腺炎大鼠胰腺中的表达

Expressions of high mobility group box 1 in acute pancreatitis of rats

目的 探讨高迁移率族蛋白-1（HMGB1）在急性胰腺炎大鼠血清及胰腺组织中的表达及意义.方法 44只SD大鼠[（350±30）g]随机分为假手术组和实验组,实验组以5％牛黄胆酸钠胰胆管逆行注射制作急性胰腺炎大鼠模型.酶联免疫吸附试验检测外周血液中不同炎性因子的表达,Western blot法检测胰腺组织中HMGB1的蛋白表达.结果 早期炎性因子白细胞介素（IL）-1β、IL-6、肿瘤坏死因子（TNF）-α在造模3h后表达明显升高,6h达峰值,12 h后出现表达下调[IL-1β：（163.42±19.63） ng/L （6 h）,IL-6：（168.98±19.97） ng/L （6 h）,TNF-α：（1 438.60±94.78） ng/L（6 h）,P＜O.05].HMGB1在外周血清中,3h无明显表达,6h后持续升高[HMGB1：（192.46±34.29） ng/L（6 h）,P＜0.05].结论 HMGB1在急性胰腺炎中的表达晚于早期炎性因子IL-1、TNF-α、IL-6,可能在维持和促进急性胰腺炎的发生、发展中起关键作用.

Objective To study the expression of high mobility group box 1 （HMGB1） and early inflammation factors,such as interleukin （IL）-1,IL-6,tumor necrosis factor （TNF）-αr in serum and pancreatic tissues of rats with acute pancreatitis.Methods Forty-four SD male rats （350 ± 30 g） were divided into sham-operated group （SO group）,experimental group （ANP）.The rat acute pancreatitis model was established by retrograde injeetion of 5% sodium tauroeholate into the biliopancreatic duct.The expression of different inflammation factors in serum of rats with acute panreatitis at different time points was detected by using enzyme linked immunosorbent assay （ELISA）.HMGB1 was detected by using Western blotting in pancreatic tissues of rats with acute pancreatitis tissue at different time intervals.Results The early inflammation factors were quickly increased at 3 h after the model was established,and reached a peak at 6 h,then decreased at 12 h [IL-1β：[163.42 ± 19.63） ng/L （6 h）,IL-6：（168.98 ± 19.97） ng/L （6 h）,TNF-α：（1 438.60 ±94.78） ng/L （6 h）,P〈0.05].HMGB1 showed no significant change at 3 h.However,HMGB1 levels in pancreatic tissues were increased remarkably at 6 h,and maintained up to 24 h post-acute pancreatitis [HMGB1：（192.46 ± 34.29） ng/L （6 h）,P 〈 0.05].Conclusion HMGB1,as a late inflammation factor,was different from some early inflammation factors,such as IL-1,TNF-α,IL-6,which was increased obviously at the late stage of acute pancreatitis.HMGB1 may play a key role in maintaining the development and aggravation of acute pancreatitis.