摘要目的:分析重症胰腺炎(SAP)继发感染SD大鼠模型小肠防御素-5 mRNA的变化，探讨SD大鼠肠道内感染菌情况。方法:将实验使用的36只SD健康大鼠分为4组，每组9只，分别建立SAP大鼠模型，A组为对照组，将大鼠直接处死。B、C、D组分别在制成大鼠模型后12、24、36 h后对大鼠进行处死，对胰腺进行病理性检查，采用反转录-聚合酶链反应(RT-PCR)技术观察大鼠模型体内小肠防御素-5 mRNA的水平变化，观察大鼠腹水颜色、胰腺组织病理学、胰腺大体组织学、血清脂肪酶含量、血清淀粉酶含量、大鼠肠道内感染菌情况。结果:B、C、D组健康SD大鼠均患SAP；运用RT-PCR技术得出B、C、D组小肠防御素-5 mRNA水平分别为0.769±0.090、0.571±0.129、0.510±0.063，均低于A组(1.107±0.164， t＝5.420、6.269、10.194， P<0.05)。B、C、D组SD大鼠与A组比较，腹水颜色更深，胰腺组织破坏更明显；B、C、D组大鼠血清脂肪酶含量分别为(2 177.84±86.36)、(2 348.79±83.45)、(2 459.87±91.36) U/L，血清淀粉酶含量分别为(7 767.94±436.36)、(8 348.79±463.46)、(9 859.87±461.37) U/L均高于A组的(107.71±36.17)、(1 446.71±236.14) U/L(血清脂肪酶： t＝66.330、73.921、71.815， P<0.05；血清淀粉酶： t＝38.221、39.808、48.700， P<0.05)；大鼠肠道内均受到细菌感染，且细菌菌株随着大鼠病情加重而增多( P<0.05)。 结论:SD大鼠模型小肠防御素-5 mRNA获得性缺陷是造成SAP大鼠体内胰腺组织损坏、受到细菌感染的重要因素。

abstractsObjective:To analyze the changes of defensin-5 mRNA in small intestine of SD rats with secondary infection of severe pancreatitis (SAP), and to study the situation of intestinal infection bacteria in SD rats.Methods:Totally, 36 SD healthy rats were divided into 4 groups, 9 rats in each group. SAP rat models were established. The group A was the routine group, and the rats were killed directly. The rats in groups B, C and D were killed at 12, 24 and 36 h after the model was made. The pancreas was examined pathologically. The level of small intestinal defensin-5 mRNA in the model was observed by reverse transcription-polymerase chain reaction (RT-PCR). The ascites color, pancreatic histopathology, pancreatic gland gross histology, serum lipase content, serum amylase content and intestinal infection bacteria were observed.Results:The mRNA levels of defensin-5 in groups B, C and D were 0.769±0.090, 0.571±0.129 and 0.510±0.063 respectively, which were lower than those in group A (1.107±0.164, P<0.05). Compared with group A, SD rats in groups B, C and D had darker ascites and more obvious pancreatic tissue destruction. Serum lipase contents in groups B, C and D were (2 177.84±86.36), (2 348.79±83.45), (2 459.87±91.36) U/L, and serum amylase contents were (7 767.94±436.36), (8 348.79±463.46), (9 859.87±461.37) U/L, respectively, which were significantly higher than those in group A [(107.71±36.17), (1 446.71±236.14) U/L ( P<0.05)]. The intestinal tract of rats were infected with bacteria, and the bacterial strains increased with the severity of the disease ( P<0.05). Conclusion:The acquired deficiency of defensin-5 mRNA in the small intestine of SD rats is an important factor that causes pancreatic tissue damage and bacterial infection in SAP rats.