Overexpressed microrna-129-5p reverses CCl4-Induced hepatic fibrosis by suppressing PEG3 expression and the NF-κB signaling pathway

Hepatic fibrosis is a pathological process resulting from liver damage, which leads to the extracellular matrix (ECM) proteins accumulation in the liver. Considering that microRNA (miR)-129-5p has a vital effect in the gene expression regulation about fibrosis through transcriptional profiling, this study speculated whether miR-129-5p had potential to influence the progression of hepatic fibrosis. The hepatic fibrosis rat models induced by C-C motif chemokine ligand 4 (CCl4) were established. The pathological changes of the liver tissues were assayed with hematoxylin-eosin (HE) staining. Subsequently, gain- and loss-of-function analysis with miR-129-5p antagomir or shRNA against PEG3 was conducted to further investigate the molecular regulatory mechanism of miR-129-5p, with detection of the expression of NF-{kappa}B signaling pathway-related proteins and apoptosis-related factors. The serum samples of rats were analyzed by serological index analysis. The targeting of miR-129-5p to PEG3 was verified by dual-luciferase reporter gene assay. The detection of apoptosis in rats was measured by TUNEL staining. MiR-129-5p was poorly-expressed and PEG3 was highly-expressed in hepatic fibrosis. miR-129-5p could reduce the expression of PEG3. Next, upregulated miR-129-5p or downregulated PEG3 led to less obvious histological changes of liver cirrhosis and lowered apoptosis rate. Further, miR-129-5p regulated the activation of NF-{kappa}B signaling pathway via PEG3. The hepatic fibrosis induced by CCl4 can be reversed by upregulated miR-129-5p or downregulated PEG3 expression.