inhibits hepatic fibrosis and hepatic stellate cell activation by targeting the PI3K/Akt/mTOR pathway.
Zhiheng Dong, Haibin Guan, Lu Wang, Lijuan Liang, Yifan Zang, Lan Wu, Lidao Bao
Author Information
Zhiheng Dong: Department of Pharmacy, Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region 010030, P.R. China.
Haibin Guan: College of Pharmacy, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region 010110, P.R. China.
Lu Wang: College of Basic Medicine, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region 010110, P.R. China.
Lijuan Liang: College of Pharmacy, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region 010110, P.R. China.
Yifan Zang: College of Pharmacy, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region 010110, P.R. China.
Lan Wu: Mongolia Medical School, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region 010110, P.R. China.
Lidao Bao: Department of Pharmacy, Hohhot First Hospital, Hohhot, Inner Mongolia Autonomous Region 010030, P.R. China.
Hepatic fibrosis (HF) is a process that occurs during the progression of several chronic liver diseases, for which there is a lack of effective treatment options. (CTL) is often used in Chinese or Mongolian medicine to treat liver diseases. However, its mechanism of action remains unclear. In the present study, CTL was used to treat rats with CCl4‑induced HF. The histopathological, biochemical and HF markers of the livers of the rats were analyzed, and CTL‑infused serum was used to treat hepatic stellate cells (HSCs) in order to detect the relevant markers of HSC activation. Protein expression pathways were detected both and . Histopathological results showed that CTL significantly improved CCl4‑induced liver injury, reduced aspartate aminotransferase and alanine aminotransferase levels, promoted E‑cadherin expression, and decreased α‑smooth muscle actin (SMA), SOX9, collagen I and hydroxyproline expression. Moreover, CTL‑infused serum was found to decrease α‑SMA and collagen I expression in HSCs. Further studies showed that CTL inhibited the activity of the PI3K/Akt/mTOR pathway in the rat livers. Following the administration of the PI3K agonist 740Y‑P to HSCs, the inhibitory effect of CTL on the PI3K/Akt//mTOR pathway was blocked. These results suggested that CTL can inhibit HF and HSC activation by inhibiting the PI3K/Akt/mTOR pathway.
