摘要
目的探讨甲基化CpG结合蛋白(MeC P2)对小鼠肺泡巨噬细胞MH-S分泌炎症因子的作用。方法采用MeC P2-siRNA抑制MeC P2表达,使用Q-PCR、ELISA和Western blot方法检测MeC P2、白介素(IL)-1β、IL-6、肿瘤坏死因子(TNF)-α、p-p65和p-IκBα的表达情况。结果 QPCR和ELISA结果显示脂多糖(LPS)能够诱导MH-S分泌炎症因子IL-1β、IL-6和TNF-α,并且MeC P2表达也随之显著升高(P<0.01)。使用MeC P2-siRNA抑制MeC P2表达后,炎症因子IL-1β、IL-6和TNF-α表达明显降低,同时pp65和p-IκBα表达也显著下调(P<0.01)。结论抑制MeC P2表达能够抑制LPS刺激MH-S细胞分泌炎症因子,可能是通过抑制NF-κB的活化,但具体机制尚需进一步研究。
Objective To study the effect of methyl-Cp G-binding protein 2（ MeCP2） on inflammatory cytokines secreted in alveolar macrophages of mice. Methods MeCP2-siRNA was used to inhibit the expression of MeCP2,and the expression of MeCP2,interleukin（ IL）-1β,IL-6,tumor necrosis factor,（ TNF）-α,p-p65 and p-IκBαwere detected by Q-PCR,ELISA and Western blot. Results Q-PCR and ELISA showed that lipopolysaccharide（ LPS） could induce expression of IL-1β,IL-6 and TNF-α,and the expression of MeCP2 also increased significantly in MH-S cells（ P〈0. 01）. The expression of IL-1β,IL-6 and TNF-α was down-regulated by MeCP2-siRNA（ P〈0. 01）,and the expression of p-p65 and p-IκBα was also down-regulated in MH-S（ P〈0. 01）. Conclusion Inhibition of MeCP2 expression could inhibit the secretion of inflammatory cytokines by LPS stimulating MH-S cells,possibly through inhibiting NF-κB activation,however,the specific mechanism needs further study.
出处
《安徽医科大学学报》
CAS
北大核心
2018年第5期734-738,共5页
Acta Universitatis Medicinalis Anhui
基金
国家自然科学基金青年科学基金(编号：81100302)
