外源性IL-10对急性坏死性胰腺炎大鼠胰腺及肝组织STAT3表达的影响

Exogenous IL-10 downregulates STAT3 expression in pancreatic and hepatic tissue of rats with acute necrotizing pancreatitis

目的:探讨外源性人重组白介素10(IL-10)在急性坏死性胰腺炎(ANP)大鼠胰腺及肝组织中对信号转导和转录激活因子3(STAT3)表达的影响.方法:92只健康SD♂大鼠随机分为正常对照组(C组,n=24)、ANP组(A组,n=36)和IL-10后干预组(I组,n=32).采用腹腔注射左旋精氨酸(L-arginine)的方法诱导大鼠ANP模型,注射L-arginine后2、5、8h,腹腔注射重组IL-1010000U干预后,分别于4、12、24、36h分批处死各组大鼠,苏木精-伊红染色(HE)观察大鼠胰腺及肝组织病理学变化,快捷免疫组织化学MaxVisionTM法检测在胰腺和肝组织中STAT3的表达变化.结果:A组、I组各时点胰腺病理学评分显著高于C组(均P<0.01),12、24、36h的I组胰腺评分较A组低(均P<0.05).肝组织A组各时点病理学评分均显著高于C组(均P<0.05或0.01);I组肝脏病理评分高于C组(均P<0.05或0.01),除24h较A组下降以外,其余各时点与A组无差异.胰腺组织和肝组织的A组、I组各时点STAT3灰度值均显著低于C组(P<0.01);I组胰腺12、24、36h的STAT3灰度值显著高于A组(12h:174.61±6.25vs146.10±10.51;24h:178.55±10.36vs150.63±9.11;36h:193.37±21.54vs155.55±11.70,均P<0.05或0.01).I组肝组织24、36h的STAT3灰度值显著高于A组(24h:89.88±18.89vs38.85±10.27;36h:48.79±15.38vs23.51±5.67,均P<0.01).结论:外源性IL-10后干预对ANP胰腺及肝组织损伤有一定保护作用,STAT3可能早期即参与ANP胰腺和肝脏组织的炎症反应,IL-10可能通过抑制STAT3途径对胰腺、肝组织起保护作用.

AIM：To investigate the effect of treatment with exogenous interleukin-10（IL-10） on the expression of signal transducer and activator of transcription3（STAT3） in pancreatic and hepatic tissue of rats with acute necrotizing pancreatitis（ANP）.METHODS：Ninety-two male Sprague-Dawleyrats were divided randomly into three groups：control group（n=24）,ANP group（n=36）,andIL-10 group（n=32）.ANP was induced in ratsby intraperitoneal injection（ip） of L-arginine.The IL-10 group was treated with 10 000 unitsof recombinant human IL-10（rhIL-10） by ip at 2,5,and 8 h after the last L-arginine injection.Rats were killed at 4,12,24,and 36 h after the last L-arginine injection.Pancreatic and hepatic histopathological changes were scored,and the expression of STAT3 was detected by immunohistochemical（IHC） staining.RESULTS：Pancreatic and hepatic histopathological scores at all time points were significantly higher in the ANP group and IL-10 group than in the control group（all P0.01 or 0.05）.Compared to the ANP group,pancreatic histopathological scores at 12,24,and 36 h and hepatic histopathological score at 24 h were signif icantly lower in the IL-10 group（all P0.05 or 0.01）.The expression levels of STAT3 in pancreatic and hepatic tissue at all time points were significantly lower in the ANP group and IL-10 group than in the control group（all P0.01）.The expression levels of STAT3 in pancreatic（12 h：174.61 ± 6.25 vs 146.10 ± 10.51;24 h：178.55 ± 10.36 vs 150.63 ± 9.11;36 h：193.37 ± 21.54 vs 155.55 ± 11.70,all P0.01 or 0.05） and hepatic tissue（24 h：89.88 ± 18.89 vs 38.85 ± 10.27;36 h：48.79 ± 15.38 vs 23.51 ± 5.67,all P0.01） were significantly higher in the IL-10 group than in the ANP group.CONCLUSION：STAT3 may be involved in the early in？ ammatory response to ANP.Exogenous IL-10 could improve pancreatic and hepatic tissue injury in ANP rats possibly by downregu-lating STAT3 expression.