白细胞介素11调控大鼠NEC肠道增殖与凋亡的分子机制研究

Mechanisms investigation of IL-11 in the regulation of proliferation and apoptosis of intestinal epithelial cells in rats with NEC

目的研究白细胞介素11(IL-11)调控大鼠坏死性小肠结肠炎(NEC)肠道增殖与凋亡的分子机制研究。方法实验分为正常对照组、NEC组和IL-11治疗组。1.细胞凋亡(TUNEL)法检测IL-11对大鼠肠上皮细胞凋亡的影响。2.免疫组织化学法检测IL-11对Bax、Bcl-2和增殖细胞核抗原(PCNA)表达变化的影响。数据采用SPSS 13.0软件统计分析。细胞凋亡表达变化和病理图像分析MOD值的变化以均数±标准差(±s)表示,One-Way-ANOVA方差分析,P<0.01表示差异有统计学意义。结果 1.细胞凋亡变化:正常对照组肠上皮细胞核为弱阳性;NEC组绝大部分细胞核呈棕色,为强阳性;IL-11治疗组大部分呈棕色,呈阳性。定量分析表明NEC时肠上皮细胞凋亡显著增加,IL-11能显著减少凋亡。2.免疫组织化学法定量:NEC时肠上皮细胞Bax表达增加,Bcl-2、PCNA表达下降,表明IL-11能显著下调Bax,上调PCNA、Bcl-2的表达,差异均有统计学意义(P<0.01)。结论肠上皮细胞凋亡在NEC显著增加,外源性IL-11能显著减轻肠道损伤,促进修复。其机制与IL-11下调Bax,上调Bcl-2、PCNA的表达有关。

Objective To investigate molecular mechanisms of interleukin 11 （ IL-11 ） in the regulation of proliferation and apoptosis of intestinal epithelial cells in rats with NEC . Methods Rats were randomly divided into control group , NEC group and IL-11 treatment group.1.TUNEL was performed to detect the apoptosis of intestinal epithelial cells in rats .2.The expression of Bax , Bcl-2 and PCNA were detected by immunohistochemistry staining .Measurement data were represented as mean ＆#177;SD （ x＆#177;s ） and were examined by using One-Way-ANOVA analysis of variance .Statistical analysis were performed by using SPSS 13.0 software. Results Firstly, concerning intestinal epithelial cells apoptosis , in control group intestinal epithelial cell nucleus was weak positive , while the majority of the nucleus of intestinal epithelial cell in NEC group was brown （ strongly positive ） , and in IL-11 treatment group the nucleus of intestinal epithelial cell was mostly brown （positive）.The quantitative analysis showed that the apoptosis of intestinal epithelial cells was significantly increased in NEC rats , and IL-11 could significantly decrease the apoptosis . Secondly , in NEC group the expression of Bax in intestinal epithelial cells was increased and the expression of PCNA and Bcl-2 was decreased , which indicated that IL-11 could significantly downregulate the expression of Bax, and upregulate the expression of PCNA and Bcl-2. Conclusion Apoptosis of intestinal epithelial cells are significantly increased in NEC rats .exogenous interleukin 11 could significantly reduce intestinal injury and could promote the repair .The molecular mechanism might be that IL-11 could downregulate the expression of Bcl-2 and could upregulate Bax , PCNA.