肿瘤坏死因子在大鼠重症急性胰腺炎并发肾损伤时的表达变化

Expression of tumor necrosis factor-α in rats with severe acute pancreatitis complicated with acute renal injury

目的探讨重症急性胰腺炎并发急性肾损伤时肿瘤坏死因子（TNF）-α dmRNA表达变化及其机制。方法将32只健康SD大鼠随机分为两组：假手术组（n=16）、胰腺炎组（n=16）。假手术组开腹仅翻动肠管；胰腺炎组经胆胰管逆行注射3％牛磺胆酸钠（0．05ml／kg）建立大鼠SAP模型。分别于制模后12、24h采血测定血清淀粉酶活性，血清尿素氮、肌酐浓度和肾脏组织TNF-α mRNA表达变化，观察胰腺及肾脏病理形态学改变。结果胰腺炎组大鼠血清淀粉酶活性（1046．45±453、37、1916．50±461．91），血清尿素氮（23．49±3．12、39．79±3．51）、肌酐浓度（171．38±43．26、216．25±21．76）及肾组织TNF-α mRNA表达水平均较假手术组明显升高。胰腺及肾脏病理损害严重，腹水的生成（8．89±2．16、12．87±3．17）和皂化斑的形成较多；假手术组未见明显异常。结论SD大鼠SAP时肾组织TNF-α mRNA表达水平明显升高，提示肾脏组织TNF-α在SAP合并急性肾损伤的发病机制中起重要作用。

Objective To explore the expression changes of tumor necrosis factor （TNF）-α mRNA in severe acute pancreatitis （SAP） complicated with acute renal injury （ ARI ） and the mechanisms. Methods Thirty-two healthy SD rats were randomly divided into two groups： sham operation group （ n =16）, and pancreatitis model group （ n =16）. In sham operation group, the rats were subjected to abdomen opening and intestinal canal tipping only. In pancreatitis model group, the model of SAP was induced by retrograde injection of 3 % sodium taurocholate into biliopancreatic duct, and rats were sacrificed at 12 and 24 h after modeling. The eoneentrations of serum amylase, serum urea nitrogen, creatinine, and the expression of TNF-α mRNA in renal tissues were detected. Pathologie changes in the kidney and pancreas were observed under a light microscope. Results The concentrations of serum amylase （ 1046.45 ± 453.37, 1916. 50 ±461.91）, serum urea nitrogen （23.49±3.12, 39. 79 ±3.51）, creatinine （171.38 ± 43. 26, 216. 25±21.76） and the expression of TNF-α mRNA in the renal tissues were significantly higher in pancreatitis group than in sham operation group： Pathological lesions in the liver and kidney were deteriorated, and ascite and saponification were increased in pancreatitis group. No abnormal ehanges were found in sham operation group. Conclusion The expression of TNF-α mRNA in the renal tissues was significantly up-regulated in SD rats with SAP, suggesting the vital roles of TNF-α in the renal tissues in the pathogenesis of SAP complicated with ARI.