Liver fibrosis is a common pathological process in the progression of several chronic liver diseases to cirrhosis and hepatocellular carcinoma. Therefore, the development of medications that can repress the progress of liver fibrosis is essential. We discovered that initially, 12β-( m -methyl-benzoyl)-11,12-dihydro oleanolic acid (12d-OA), a farnesoid X receptor (FXR) modulator, possessed potential anti-fibrotic properties. Through an in-depth study, we revealed that 12d-OA not only inhibited the expression of fibrogenic markers in the LX-2 cells and HSC-T6 cells but also exhibited significant protective effects against liver injury and liver fibrosis in bile duct ligation (BDL) rats. Further exploration of its molecular mechanism indicated that 12d-OA exerted antifibrotic activity by inhibiting the extracellular signal-regulated kinase (ERK)/stress-activated protein kinase (p38) signaling pathways. Consequently, the great effects of 12d-OA in vitro and in vivo suggest that it may be a good candidate for liver fibrosis.
Keyphrases
- liver fibrosis
- signaling pathway
- induced apoptosis
- liver injury
- pi k akt
- drug induced
- knee osteoarthritis
- protein kinase
- cell cycle arrest
- epithelial mesenchymal transition
- binding protein
- transcription factor
- cell death
- idiopathic pulmonary fibrosis
- oxidative stress
- single cell
- optical coherence tomography
- risk assessment
- climate change
- stress induced