| Literature DB >> 32348814 |
Si Chen1, Shuhua Yang2, Mingyang Wang3, Jia Chen4, Sheng Huang5, Zhen Wei6, Ziyang Cheng7, Hanli Wang8, Miao Long9, Peng Li10.
Abstract
The toxic effect of zearalenone (ZEA) is not fully understood and there is an urgent need for the development of effective agents to protect against the toxic effects of ZEA. In this study, we detected whether curcumin (CUR) can reduce Leydig cells apoptosis induced by ZEA. The Effects of ZEA and CUR on cell viability was evaluated using a Cell Counting kit-8 assay (CCK-8). Apoptosis was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay and flow cytometry. The protective effect of CUR on oxidative stress induced by ZEA was determined by ROS, MDA, T-SOD, GSH and GSH-Px levels. In addition, we also determined effects of key signaling pathways and proteins involved in the apoptotic, PI3K-AKT, Nrf2 and endoplasmic reticulum stress signaling pathways by Western blotting. The expressions of proteins (PTEN, AKT, p-AKT, Bax, Bcl-2, GRP78, CHOP, JNK, P-JNK, Caspase-12, Caspase-9, Caspase-3, Nrf2, Keap1 and HO-1) were measured. The experimental results showed that CUR can alleviate oxidative stress and apoptosis caused by ZEA through the PI3K-AKT, Nrf2 and endoplasmic reticulum stress signaling pathways. Our results provide a theoretical basis for molecular studies of ZEA toxicology and clinical application of CUR.Entities:
Keywords: Curcumin; Endoplasmic reticulum stress; Leydig cell; Nrf2 signaling pathway; PI3K-AKT signaling Pathway; Zearalenone
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Year: 2020 PMID: 32348814 DOI: 10.1016/j.fct.2020.111385
Source DB: PubMed Journal: Food Chem Toxicol ISSN: 0278-6915 Impact factor: 6.023