Oncotarget

Research Papers:

Resveratrol alleviates FFA and CCl4 induced apoptosis in HepG2 cells via restoring endoplasmic reticulum stress

Fenghua Li, Yang Yang, Lili Yang, Kai Wang, Xing Zhang, Yunlong Zong, Yixin Ding, Changhong Wang, Li Zhang and Guang Ji _

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Oncotarget. 2017; 8:43799-43809. https://doi.org/10.18632/oncotarget.16460

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Abstract

Fenghua Li1,*, Yang Yang1,*, Lili Yang2, Kai Wang1, Xing Zhang1, Yunlong Zong1, Yixin Ding1, Changhong Wang3, Li Zhang2 and Guang Ji1,2

1Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, China

2Institute of Digestive Diseases, China-Canada Center of Research for Digestive Diseases, Shanghai University of Traditional Chinese Medicine, Shanghai, China

3Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China

*These authors contributed equally to this work

Correspondence to:

Li Zhang, email: [email protected]

Guang Ji, email: [email protected]

Keywords: apoptosis, endoplasmic reticulum stress, resveratrol, inflammation, cytokines

Received: January 18, 2017     Accepted: March 15, 2017     Published: March 22, 2017

ABSTRACT

Cell apoptosis often induces inflammation and injury in the liver, with endoplasmic reticulum (ER) stress as the most possible reason. Resveratrol (RSV) has been shown to prevent hepatic steatosis and alleviate apoptosis, however, the exact mechanisms underlying the effects still need to be explored. Here we co-cultured HepG2 cells with free fatty acid (FFA) solution (oleic acid: palmitic acid = 2:1) and then exposed to a carbon tetrachloride (CCl4) solution to induce apoptosis. To evaluate the therapeutic effects, RSV (2.5 μM, 5 μM, 10 μM) was added to the cells. Results showed that HepG2 cells co-cultured with FFA exhibited lipid infiltration and were susceptible to apoptosis upon exposure to the CCl4 solution. The expression of molecules related to apoptosis (Caspases, Bcl-2/Bax) and ER stress (GRP78, IRE1, ATF6, PERK, et al.) was all significantly decreased upon RSV treatment. We further inhibited GRP78 by siRNA, results showed that the anti-apoptotic effect of RSV still maintained under GRP78 siRNA condition. Our data demonstrated that lipid accumulated HepG2 cells were susceptible to injury, and RSV could improve apoptosis in FFA and CCl4 stressed cells, which partially via restoring ER function.


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