BACKGROUND Liver fibrosis is the response of liver diseases that puzzles patients. MiRNAs were involved in the regulating processes of liver fibrosis. This study aims to investigate the effects of ARRB1 mediated by miR-29a and miR-652 on liver fibrosis and its possible mechanism. METHODS Liver fibrosis of mice was induced by intraperitoneal injection of CCl4. Liver function was observed by the levels of alanine transaminase (ALT) and aspartate transaminase (AST). Flow cytometry was used to detect the percent of T helper17 (Th17). ELISA (Enzyme linked immunoassay) was used to detect the levels of Interleukin-17 (IL-17) and Interleukin-22 (IL-22). Real-time PCR was used to detect the expression of IL-17A, IL-22, miR-29a, miR-652 and β-Arrestin 1 Gene (ARRB1). Western blot was used to detect the protein expression of ARRB1. RESULTS CCl4 supplementation significantly increased the level of ALT and AST, the percent of Th17, the level of IL-17A, IL-22, miR-29a and miR-652, but decreased ARRB1. Overexpression of miR-29a/miR-652 prominently decreased Th17, IL-17A, IL-22 and ARRB1 in the normal CD4+ T cells. Both miR-29a and miR-652 targeted ARRB1 to regulate its expression. The effects of miR-29a/miR-652 overexpression on CD4+ T cells were reversed by ARRB1 overexpression. In vivo experiments demonstrated the protective role of miR-29a/miR-652 overexpression on liver fibrosis. CONCLUSION ARRB1 mediated by miR-29a and miR-652 probably involved in the CD4+ T cells differentiation in patients with liver fibrosis, and functioned as a biomarker of fibrosis liver.Key words: liver fibrosis, miR-29a, miR-652, ARRB1, CD4+ T cells.

中文翻译：

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MiR-29a和miR-652通过抑制CD4 + T细胞的分化来减轻肝纤维化。

背景技术肝纤维化是使患者困惑的肝脏疾病的反应。MiRNA参与肝纤维化的调节过程。本研究旨在探讨miR-29a和miR-652介导的ARRB1对肝纤维化的作用及其可能的机制。方法腹腔注射四氯化碳可致小鼠肝纤维化。通过丙氨酸转氨酶（ALT）和天冬氨酸转氨酶（AST）的水平观察肝功能。流式细胞仪用于检测T辅助蛋白17（Th17）的百分比。ELISA（酶联免疫测定）用于检测白介素17（IL-17）和白介素22（IL-22）的水平。实时荧光定量PCR检测IL-17A，IL-22，miR-29a，miR-652和β-Arrestin1基因（ARRB1）的表达。用蛋白质印迹法检测ARRB1的蛋白表达。结果CCl4的添加显着增加了ALT和AST水平，Th17的百分比，IL-17A，IL-22，miR-29a和miR-652的水平，但降低了ARRB1。在正常CD4 + T细胞中，miR-29a / miR-652的过表达显着降低了Th17，IL-17A，IL-22和ARRB1。miR-29a和miR-652均靶向ARRB1来调节其表达。ARR1过表达逆转了miR-29a / miR-652过表达对CD4 + T细胞的影响。体内实验证明了miR-29a / miR-652过表达对肝纤维化的保护作用。结论miR-29a和miR-652介导的ARRB1可能参与了肝纤维化患者的CD4 + T细胞分化，并具有肝纤维化的生物标志物的作用。关键词：肝纤维化，miR-29a，miR-652，ARRB1， CD4 + T细胞。