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目的:探讨miR-193a对刀豆蛋白a(Concanavalin A，Con a)所致小鼠慢性肝损伤的影响及其分子机制。方法:c57BL/6小鼠32只，随机分成对照组、ConA损伤组、过表达组(ConA＋慢病毒包装miR-193a组)、过表达对照组(ConA＋慢病毒空载体组)，每组8只；小鼠经尾静脉按8 mg/kg体重每周注射ConA 1次(对照组注射等体积生理盐水)，连续8周，构建慢性肝损伤模型，过表达组第6周于ConA给药48 h后经尾静脉将慢病毒包装的miR-193a过表达质粒注射到小鼠体内，过表达对照组以相同的给药方式注射慢病毒空载体(对照组、ConA损伤组注射等体积生理盐水)；ConA给药8周后，处死小鼠收集样本，血清酶学谷丙转氨酶(alanine aminotransferase ，AST)和谷草转氨酶(aspartate aminotransferase ，ALT)水平、HE染色及Masson染色评价模型小鼠实验性肝损伤程度，实时荧光定量逆转录聚合酶链反应(real time fluorescent quantitative reverse transcription polymerase chain reaction，qRT-PCR)检测miR-193a，Ⅰ型胶原(collage type Ⅰ，col1a1)，Ⅳ型胶原(collage type Ⅳ，col4a1)，α-平滑肌激动蛋白(α-smooth muscle actin，α-SMA)和激活素受体1(activin receptor-1，acvr1)，激活素a(activin a)，smad 2 mRNA的表达，Westernblot检测col1a1和α-SMA蛋白的表达；KEGG分析miRNA在多种信号通路中的富集，GO分析miR-193a作用靶基因的生物学作用，在线生物信息学预测miR-193a与acvr1之间的靶向结合作用。结果:慢性肝损伤模型中miR-193a表达明显下调(n F＝7.044，n P<0.05)。在肝损伤鼠体内过表达miR-193a后，AST和ALT含量明显下降(n t值分别为2.733和6.412，n P值均<0.05)，HE和Mass染色检测观察到过表达的miR-193a明显减轻肝损伤的程度，抑制与肝损伤相关col1a1，col4a1和α-SMA表达(n F值分别为5.295，6.443，8.546，n P值均<0.05)。通过生物信息学分析miR-193a与acvr1之间存在的潜在的预测靶点，miR-193a过表达后下调acvr1，和activin a和smad 2 mRNA的表达(n F值分别为6.046，7.716，7.063，n P值均<0.05)。n 结论:miR-193a可通过抑制activin/smad信号通路中acvr1的表达，减轻ConA诱导的慢性实验性肝损伤。“,”Objective:To explore the effect of miR-193a on Concanavalin A(ConA) -induced chronic liver injury in mice and its molecular mechanism.Method:32 c57BL/6 mice were randomly divided into a control group, ConA injury group, overexpression group (ConA+ lentiviral packaging miR-193a group), and overexpression control group (ConA+ lentiviral empty vector group); eight of every group. ConA was injected intravenously at 8 mg/kg body weight once a week (the control group was injected with an equal volume of saline) for 8 consecutive weeks to build a chronic liver injury model. The overexpression group which the miR-193a overexpression plasmid packaged with chronic disease was injected into mice was administered via the tail vein 48 hours after ConA was administered at week 6 , and the overexpression control group was injected with the lentiviral empty vector in the same way (control group, ConA injury group were injected with equal volume of normal saline); ConA administration After 8 weeks, the mice were sacrificed to collect samples, serum AST and ALT levels were detected by enzymology, HE staining and Masson staining were used to evaluate the degree of experimental liver injury in model mice. qRT-PCR was used to detect miR-193a, collage type Ⅰ(col1a1), collage type Ⅳ(col4a1), α-smooth muscle actin(α-SMA)and activin receptor-1(acvr1), activin a, smad 2 mRNA expression, Westernblot detection of col1a1 and α-SMA protein expression; KEGG analysis of miRNA enrichment in multiple signaling pathways, GO analysis of the role of miR-193a in the target gene biology , Online bioinformatics predicts the targeted binding between miR-193a and acvr1.Results:The expression of miR-193a was significantly down-regulated in chronic liver injury models(n F=7.044, n P<0.05). After overexpression of miR-193a in mice with liver injury, the serum enzymatic alanine aminotransferase (AST) and aspartate aminotransferase (ALT) levels decreased significantly(n t valves were 2.733 and 6.412 respectively both n P values <0.05). HE and Mass staining showed that the overexpression of miR-193a significantly reduced the degree of liver injury ( n F=7.044, n P<0.05), inhibit the expression of col1a1, col4a1 and α-SMA related to liver injury(n F valves were 5.295, 6.443, 8.546 respectively, all n P values <0.05). Through bioinformatics analysis of the potential predictive targets between miR-193a and acvr1, miR-193a overexpression down-regulates the expression of acvr1, activin a and smad 2 mRNA( n Fvalves were 6.046, 7.716 and 7.063 respectively, all n P values <0.05).n Conclusion:miR-193a can reduce the ConA-induced experimentalliver injury by inhibiting the expression of acvr1 in the activin/smad signaling pathway.