Crocetin Protected Human Hepatocyte LO2 Cell From TGF-β-Induced Oxygen Stress and Apoptosis but Promoted Proliferation and Autophagy AMPK/m-TOR Pathway.

Objective: To investigate the protective effects of crocetin against transforming growth factor-β (TGF-β)-induced injury in LO2 cells.

Methods: Human hepatocyte LO2 cells were pre-treated with crocetin (10 μM) for 6, 12, and 24 h, and then induced by TGF-β. Proliferation, oxidative stress, apoptosis, autophagy, and related proteins were assessed.

Results: Crocetin pre-treating promoted proliferation but suppressed apoptosis in TGF-β-induced LO2 cells. Crocetin protected LO2 cells from TGF-β-induced inflammation and oxygen stress by reducing reactive oxygen species (ROS) and malondialdehyde (MDA) but enhancing superoxide dismutase (SOD) and glutathione (GSH). Autophagy was suppressed in TGF-β but crocetin promoted autophagy in LO2 cells by mediating Adenosine 5'-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (m-TOR) signaling pathway upregulating p-AMPK and p-Beclin-1 but downregulating p-mTOR.

Conclusions: Crocetin protected LO2 cells from TGF-β-induced damage by promoting proliferation and autophagy, and suppressing apoptosis and anti-inflammation regulation of AMPK/m-TOR signaling pathway.