HMGB1在大鼠重症胰腺炎损伤器官中的表达研究

目的观察高迁移率族蛋白1（HMGB1）在牛磺胆酸钠诱导的大鼠重症急性胰腺炎（SAP）损伤后各组织的表达情况。方法将36只SD大鼠分为假手术对照组（n=18）、SAP组（n=18）,分别于24h、48h、72h三个时间点处死,每时间点6只。动物经胆胰管逆行注射5%牛黄胆酸钠诱发SAP,对照组以生理盐水代替5%牛黄胆酸钠行假手术。链霉菌抗生物素蛋白-过氧化物酶法（S-P）检测大鼠不同组织（胰腺、肝脏、胃肠道、肺脏和肾脏）的HMGB1表达情况。结果 HMGB1在假手术组大鼠的胰腺、肝脏、胃肠道、肺脏和肾脏各组织中表达很弱甚至不表达。HMGB1在SAP大鼠上述组织中存在不同程度表达增高：①除胰导管外,胰腺腺泡和胰岛周围HMGB1表达增高;②胃肠道HMGB1在3个不同时间点均明显升高,主要表达的部位集中于黏膜深部;③在不同时间点肝细胞HMGB1轻度增高,但其它部位细胞未见表达异常;④肺支气管上皮HMGB1在24h时间点轻度增高,48h、72h达到表达高峰;⑤肾脏远曲小管HMGB1在SAP不同时间点表达增高。结论本研究结果表明HMGB1可能参与牛磺胆酸钠诱导的大鼠SAP的发病过程,而血清中增高的HMGB1可能由这些受损的器官组织产生和释放。

Expression of High Mobiltiy Group Box Protein 1 in Injured Organs of Rat with Severe Pancreatitis Induced

Objective To explore the expression of high mobility group box protein 1（HMGB1）in injured organs of rat with acute severe pancreatitis（SAP）induced by sodium taurocholate.Methods Sodium taurocholate（5%）was used to induce the pancreatitis model in Sprague-Dawley rats（n=18）,which were killed at 24 h,48 h,and 72 h,respectively.Sham-operated group was as control.The expression of HMGB1 in various injured tissues was determined by Strept Actividin-Biotin Complex（SABC）method.Results SAP with severe multiple organs or tissues injury of rats was successfully induced by sodium taurocholate.Immunohistochemical assay showed sham-operated rats pancreas and other organs had no or weak detected HMGB1 protein.In SAP group,it showed that HMGB1 increasingly expressed in pancreas and other injured organ：①HMGB1 was strongly expressed at either acinus cells or the cell around the islets but not pancreatic ducts cells;②HMGB1 was sharply increasing in stomach and small intestine at 24 h,48 h and 72 h.It was strongly expressed at deep mucosa,even at the light zone of lymph node;③Hepatocytes but not other cells with slightly increasing expression of HMGB1 were observed at different time point;④After the infusion of sodium taurocholate at 24 h,weak increasing HMGB1 protein was observed in bronchial epithelium.And it sharply increased at 48 h and 72 h time point;⑤HMGB1 was increasing distal convoluted tubule.Conclusion HMGB1 may participate in the pathogenesis of STC-induced acute pancreatitis in rat,and indicate that HMGB1 may be produced and released by injured pancreas and other damaged organs.