中文摘要：

目的探讨miR-302e在原发性胆汁性肝硬化（PBC）发病机制中的可能作用。方法采用荧光定量PCR技术检测了10名健康对照者和12名PBC患者的T细胞（CD3＋）、B细胞（CD19＋）及单核细胞（CD14＋）内miR-302e的相对表达量。以100 ng/ml的LPS刺激PBC患者、健康个体的单核细胞及转染了miR-302e mimics或inhibitor的THP-1细胞,24 h后采用ELISA法检测培养基内IL-6及TNF-α浓度的变化。结果 PBC患者外周血单核细胞内miR-302e的表达量较健康个体降低（P〈0.01）。在LPS刺激的THP-1细胞中,miR-302e mimics和inhibitor分别可以抑制和促进IL-6、TNF-α的释放（P〈0.05）。在LPS刺激下,PBC患者单核细胞释放IL-6、TNF-α的能力强于来自健康个体的单核细胞（P〈0.05）。结论 miR-302e表达降低可能导致单核细胞对LPS刺激呈现高反应性,从而参与PBC发病。

英文摘要：

Objective To investigate the role of miR-302e in the pathogenesis of primary biliary cirrhosis（PBC）.Methods The relative expression levels of miR-302e in T cells（CD3＋）,B cells（CD19＋） and monocyte（CD14＋） of 10 healthy controls and 12 PBC patients were detected by RT-PCR.The THP-1 cells transfected with miR-302e mimics or inhibitors and the monocytes from PBC patients and healthy controls were treated with 100 ng/ml bacteria lipopolysaccharide（LPS）.Twenty-four hours later,the concentrations of IL-6 and TNF-α in the culture medium were measured by ELISA.Results The monocytes of PBC patients had a significantly lower miR-302e expression compared to those of healthy controls（P0.01）.miR-302e inhibitors significantly enhanced the production of IL-6 and TNF-α in THP-1 cells exposed to LPS,and miR-302e mimics significantly decreased their production（P0.05）.When treated with LPS,the monocytes from PBC patients produced significantly more IL-6 and TNF-α compared to those from healthy controls（P0.05）.Conclusion Decreased miR-302e expression in monocytes of PBC patients may enhance IL-6 and TNF-α production and thus participate in the pathogenesis of PBC.