Plantamajoside exerts antifibrosis effects in the liver by inhibiting hepatic stellate cell activation
Affiliations: Department of Pharmacy, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, Jiangsu 210004, P.R. China, Department of General Surgery, The Second Affiliated Hospital of Nantong University, Nantong, Jiangsu 226001, P.R. China
- Published online on: August 2, 2019 https://doi.org/10.3892/etm.2019.7843
Copyright: © Wang
et al. This is an open access article distributed under the
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The pathogenesis of liver fibrosis involves the activation of hepatic stellate cells (HSCs) into muscle fiber cells and fibroblasts. The aim of the current study was to investigate whether plantamajoside (PMS) exerted antifibrosis effects by affecting HSCs activation and survival during liver fibrosis, and to investigate the underlying mechanism. HSC‑T6 cells were activated by exposure to platelet‑derived growth factor BB (PDGF‑BB), and were subsequently treated with increasing concentrations of PMS (0, 20, 40, 80 and 160 µg/ml). Cell viability, apoptosis, migration and invasion were determined using the Cell Counting Kit‑8 (CCK‑8) assay, flow cytometry and the Transwell assay, respectively. Results indicated that PDGF‑BB significantly activated HSC‑T6 cells, demonstrated by increased cell proliferation, enhanced cell migration and invasion as well as increased expression of α‑smooth muscle actin (α‑SMA) and collagen type 1 α 1 (Col1α1). PMS inhibited proliferation, induced cell apoptosis and prevented cell migration and invasion in PDGF‑BB‑treated HSC‑T6 cells in what appeared to be a dose‑dependent manner. PMS appeared to dose‑dependently reduce the protein and mRNA levels of α‑SMA and Col1α1 in PDGF‑BB‑treated HSC‑T6 cells. Furthermore, the results of the present study suggested that PMS administration inhibited the protein expression of phosphorylated‑protein kinase B in what appeared to be a dose‑dependent manner. In conclusion, the data indicated that PMS exhibited an antifibrotic effect in the liver by inhibiting hepatic stellate cell activation and survival.