摘要
目的研究白细胞介素11(IL-11)在正常大鼠空肠上皮细胞(IEC-6)损伤时的抗凋亡机制。方法通过脂多糖(LPS)作用于IEC-6,建立了坏死性小肠结肠炎体外模型,加入外源性IL-11,建立IL-11治疗模型。采用免疫印迹方法研究IL-11对大鼠肠道上皮细胞磷酸化STAT3、Bax及Bcl-2蛋白含量的表达变化影响。数据以均数±标准差(x珋±s)表示,采取one-Way-ANOVA方差分析,用SPSS 11.0统计软件进行分析,P<0.01差异有统计学意义。结果定量分析结果表明,LPS致IEC-6细胞损伤时,Bax表达增强,IL-11处理可抑制Bax的表达。P-STAT3及Bcl--2蛋白含量在LPS致IEC-6细胞损伤时表达显著减少,IL-11处理可上调上述两种蛋白的表达。结论 LPS致IEC-6细胞损伤时,外源性IL-11可能激活Jak/STAT信号通路中关键分子STAT3,继而上调Bcl-2,下调Bax发挥抗凋亡作用。
Objective To investigate the anti-apoptosis effect of IL-11 on IEC-6 cell damage model. Methods In vitro NEC model was duplicated by applying lipopolysaccharide （ LPS ） to normal rat jejunum epithelial cells （IEC-6 cells ） line. A treatment group was established by the application of IL-11. The expression of phosphorylated STAT3, Bax and Bcl-2 protein in rat intestinal epithelial cells was examined by Western blotting. Data were expressed by mean ± standard deviation and analyzed by one-way ANOVA with SPSS 11.0. Results Quantitative analysis revealed that enhanced expression of Bax and IL-11 treatment could inhibit the expression of Bax, when LPS induced IEC-6 cell injury. The expression of phosphorylation STAT3 and Bcl-2 protein was decreased significantly after IEC-6 cells injury induced by LPS. The application of IL-11 could up-regulate the expression of P-STAT3 and Bcl-2 proteins. Conclusions When the IEC-6 cells injury induced by LPS, 1L-I 1 to IEC-6 cells might activate STAT3 of the Jak/STAT signal pathway. Up-regulation of Bcl-2 as well as the down-regulation of Bax in IL-11 treatment might be effective in anti-apoptosis.
出处
《中华普外科手术学杂志（电子版）》
2015年第2期42-44,共3页
Chinese Journal of Operative Procedures of General Surgery(Electronic Edition)
基金
国家自然科学基金项目(81170603)~~
