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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。
Objective To observe the expression of high mobility group box 1 (HMGB1) in tissues induced by sodium taurocholate after severe acute pancreatitis (SAP) in rats. Methods 36 SD rats were divided into sham operation control group (n = 18) and SAP group (n = 18), and were sacrificed at three time points of 24h, 48h and 72h respectively. The animal was injected with 5% sodium taurocholate via the biliary and pancreatic ducts retrogradely to induce SAP. The control group was given sham operation instead of 5% sodium taurocholate with saline. The expression of HMGB1 in different tissues (pancreas, liver, gastrointestinal tract, lung and kidney) of rats was detected by streptavidin-peroxidase method (S-P). Results HMGB1 was weakly expressed or not expressed in the pancreas, liver, gastrointestinal tract, lung and kidney tissues in the sham operation group. The expression of HMGB1 in the above tissues of SAP rats increased to some extent: ①In addition to the pancreatic duct, HMGB1 expression increased in the pancreatic acini and islet; ②The HMGB1 in gastrointestinal tract increased significantly at 3 different time points, Concentrated in the mucosa of the deep; ③ at different time points of liver cells increased slightly HMGB1, but no other parts of the expression of abnormal cells; ④ lung bronchial epithelial HMGB1 slightly increased at 24h, 48h, 72h to reach the peak expression; Tubule HMGB1 expression increased at different time points in SAP. Conclusions The results of this study suggest that HMGB1 may be involved in the pathogenesis of sodium taurocholate-induced SAP in rats. However, elevated HMGB1 in serum may be produced and released by these damaged organs.