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目的检测胆道闭锁(BA)患儿肝组织及血浆miR-200a的表达,探讨其与BA肝纤维化及肝脏炎症的关系。方法采用逆转录PCR检测26例BA组、10例正常组血浆标本miR-200a的表达,并分析其与生化指标的相关性;采用酪胺信号放大荧光原位杂交(TSA-FISH)检测14例BA及2例正常肝组织标本miR-200a的表达;根据Ishak系统对BA肝组织进行肝纤维化及炎症评分,分析肝组织miR-200a表达与肝纤维化及炎症的相关性,并分析BA血浆与肝组织miR-200a的相关性。结果BA组血浆miR-200a表达显著高于正常组,差异有统计学意义(P<0.01);BA组血浆miR-200a表达与TB、DB、ALP、γ-GT、ALT、AST没有相关性(P>0.05)。BA组肝组织miR-200a表达显著高于正常组,BA肝组织纤维化区miR-200a表达显著低于没有纤维化的肝实质区;miR-200a与BA肝纤维化进展正相关(P<0.05),而与肝脏炎症程度无关(P>0.05)。9例检测了血浆miR-200a的肝组织标本中有6例出现肝组织miR-200a表达越高,血浆miR-200a表达越高的情况。结论miR-200a可能通过上皮间质转化、Wnt/β-catenin和TGF-β信号通路调控BA肝纤维化,并可能成为预测BA肝纤维化程度的血浆标志物。
Objective To detect the expression of miR-200a in liver tissue and plasma in children with biliary atresia (BA), and to investigate the relationship between miR-200a and hepatic fibrosis and liver inflammation in BA. Methods Reverse transcription polymerase chain reaction (RT-PCR) was used to detect the expression of miR-200a in 26 cases of BA and 10 cases of normal controls. The correlation between the expression of miR-200a and the biochemical parameters was analyzed. Forty-seven cases were detected by tyrosine signal amplification fluorescence in situ hybridization (TSA-FISH) BA and two cases of normal liver tissue samples.According to Ishak system, liver fibrosis and inflammation score of BA liver tissue were analyzed and the correlation between liver tissue miR-200a expression and hepatic fibrosis and inflammation was analyzed.And BA plasma And liver tissue miR-200a correlation. Results The plasma levels of miR-200a in BA group were significantly higher than those in normal group (P <0.01). The plasma levels of miR-200a in BA group were not correlated with TB, DB, ALP, P> 0.05). The expression of miR-200a in liver tissue of BA group was significantly higher than that in normal group, and the expression of miR-200a in fibrosis area of BA group was significantly lower than that in non-fibrosis liver tissue. The positive correlation between miR-200a and the progress of hepatic fibrosis ), But not with the extent of liver inflammation (P> 0.05). Nine of the 6 liver samples detected in plasma miR-200a showed higher expression of miR-200a in liver tissues and higher expression of miR-200a in plasma. Conclusion miR-200a may regulate BA hepatic fibrosis through epithelial-mesenchymal transition, Wnt / β-catenin and TGF-β signaling pathways and may be a plasma marker for predicting the degree of hepatic fibrosis in BA.