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

Authors：Guo, Hongxing; Ruan, Chenyu; Zhan, Xiuhong; Pan, Hao; Luo, Yumei; Gao, Ke^*

Source：Frontiers in Public Health, 2022, 10: 909125.

DOI：10.3389/fpubh.2022.909125

• crocetin
• proliferation
• autophagy
• apoptosis
• inflammation
• AMPK
• m-TOR

ObjectiveTo investigate the protective effects of crocetin against transforming growth factor-beta (TGF-beta)-induced injury in LO2 cells. MethodsHuman hepatocyte LO2 cells were pre-treated with crocetin (10 mu M) for 6, 12, and 24 h, and then induced by TGF-beta. Proliferation, oxidative stress, apoptosis, autophagy, and related proteins were assessed. ResultsCrocetin pre-treating promoted proliferation but suppressed apoptosis in TGF-beta-induced LO2 cells. Crocetin protected LO2 cells from TGF-beta-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-beta but crocetin promoted autophagy in LO2 cells by mediating Adenosine 5'-monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (m-TOR) signaling pathway via upregulating p-AMPK and p-Beclin-1 but downregulating p-mTOR. ConclusionsCrocetin protected LO2 cells from TGF-beta-induced damage by promoting proliferation and autophagy, and suppressing apoptosis and anti-inflammation via regulation of AMPK/m-TOR signaling pathway.

• Institution
  南方医科大学; 5