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-  2015 

miR-33s通过靶向p38 MAPK负性调节LPS诱导的炎症反应

DOI: doi:10.7507/1671-6205.2015040

Keywords: 脂多糖, 微小RNA, p38 MAPK, 炎症因子, 单核细胞

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Abstract:

目的探讨miR-33s是否能够通过靶向p38 MAPK负性调节LPS诱导的炎症反应。 方法体外培养人单核细胞株THP-1,分别将miR-33s的拟似物(mimic,25 nmol/L)和miR-33s的抑制剂(inhibitor,25 nmol/L)转染至THP-1细胞24 h。用浓度10.0 ng/mL的LPS诱导转染后的THP-1细胞24 h,分别采用Realtime RT-PCR和Western blot方法检测细胞miR-33s及p38MAPK蛋白表达,ELISA法检测THP-1细胞培养上清液中白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)的分泌量。 结果miR-33s mimic转染组p38 MAPK蛋白表达明显减少(P<0.05),IL-1β、TNF-α、IL-6含量显著降低(P<0.05)。miR-33s inhibitor转染组p38MAPK蛋白表达明显增加(P<0.05),IL-1β、TNF-α、IL-6含量显著上升(P<0.05)。 结论LPS能诱导THP-1细胞释放IL-1β、TNF-α、IL-6;miR-33s mimic抑制炎性细胞因子的分泌。miR-33s inhibitor促进促炎性细胞因子的分泌;miR-33s可能通过靶向结合p38 MAPK的3'末端非编码区来发挥它的负性调节炎症作用

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