Baicalin inhibits PDGF-BB-induced hepatic stellate cell proliferation, apoptosis, invasion, migration and activation via the miR-3595/ACSL4 axis.

Hepatic fibrosis is a physiological response to liver injury that includes a range of cell types. The pathogenesis of hepatic fibrosis currently focuses on hepatic stellate cell (HSC) activation into muscle fiber cells and fibroblasts. Baicalin is a flavone glycoside. It is the glucuronide of baicalein, which is extracted from the dried roots of Scutellaria baicalensis Georgi. Previous work focused on the anti‑viral, ‑inflammatory and ‑tumor properties of baicalin. However, the potential anti‑fibrotic effects and mechanisms of baicalin are not known. The present study demonstrated that baicalin influenced the activation, proliferation, apoptosis, invasion and migration of platelet‑derived growth factor‑BB‑induced activated HSC‑T6 cells in a dose‑dependent manner. To investigate the anti‑fibrotic effect of baicalin, a one‑color micro (mi)RNA array and reverse transcription‑quantitative polymerase chain reaction analyses were used. Results demonstrated that baicalin increased the expression of the miRNA, miR‑3595. In addition, the inhibition of miR‑3595 substantially reversed the anti‑fibrotic effect of baicalin. The present data also suggested that miR‑3595 negatively regulates the long‑chain‑fatty‑acid‑CoA ligase 4 (ACSL4). Furthermore, ACSL4 acted in a baicalin‑dependent manner to exhibit anti‑fibrotic effects. Taken together, it was concluded that baicalin induces miR‑3595 expression that modulates the expression levels of ACSL4. To the best of our knowledge, the present study is the first to demonstrate that baicalin induces overexpression of human miR‑3595, and subsequently decreases the expression of ACSL4, resulting in an anti-fibrotic effect.