The Role and Molecular Regulatory Mechanism of A Disintegrin and Metalloprotease 9 in Alcoholic Liver Fibrosis

A disintegrin and metalloprotease 9 has been reported to play a key role in many diseases. However, the underlying effects mechanisms of alcoholic liver fibrosis have not well understood. To investigate its regulatory molecular mechanism fibrosis, single guide ribonucleic acid targeting sequence mice was adopted by clustered regularly interspaced short palindromic repeats/Cas9 technology inhibit expression this study. Subsequently, hepatic stellate cell-T6 male C57BL/6J were respectively divided into 4 groups each group treated differently. In vivo experiment, normal fed with control Lieber-DeCarli TP4030C; saline+alcohol injected saline; 9-single acid+alcohol effective plasmids c-Jun N-terminal kinase inhibitor+alcohol inhibitor SP600125. All except for received TP4030A carbon tetrachloride. Furthermore, examination serum aspartate transaminase alanine activities pathological analysis hematoxylin-eosin staining, picric acid-sirius red Hoechst 33 258 staining confirmed pro-fibro genic effect 9. Compared group, levels 9, p-c-Jun, cytochrome P450 2E1, tumor necrosis factor alpha, alpha-smooth-muscle actin Bcl-2-associated X 9- decreased significantly (p<0.05 or p<0.01), while heat shock protein 70, proliferating cell nuclear antigen vascular endothelial growth increased p<0.01). addition, vitro experiment could proliferation cells promote apoptosis. Collectively, our results indicated that activating signaling pathway, which is expected make breakthrough gene therapy fibrosis.