期刊
FOOD & FUNCTION
卷 12, 期 21, 页码 10741-10749出版社
ROYAL SOC CHEMISTRY
DOI: 10.1039/d1fo00478f
关键词
-
资金
- Key Program of Natural Science Foundation of Heilongjiang Province of China [ZD2021C003]
- National Natural Science Foundation of China [32172932]
- China Agriculture Research System of MOF and MARA [CARS-35]
The study demonstrates the protective role of lycopene in preventing DEHP-induced hepatic toxicity by regulating mitochondria-endoplasmic reticulum (ER) coupling.
Di (2-ethylhexyl) phthalate (DEHP) is a hazardous compound used as a plasticizer in plastic products. As a natural carotenoid, lycopene (LYC) is considered an effective protective agent against various types of organ damage. The present study aimed to investigate the role of mitochondria-endoplasmic reticulum (ER) coupling in LYC preventing DEHP-induced hepatotoxicity. The mice were treated with LYC (5 mg kg(-1)) and/or DEHP (500 or 1000 mg kg(-1)). In the present study, LYC prevented DEHP-induced histopathological changes including fibrosis and glycogen storage in the liver. Additionally, LYC alleviated DEHP-induced ultrastructural injury of mitochondria and ER. LYC had the underlying preventability against DEHP-induced mitochondrial dynamics imbalance including an increase in fission and a decrease in fusion. Furthermore, DEHP induced mitochondria-associated endoplasmic reticulum membrane (MAM) disorder-induced ER stress through the ER unfolded protein response (UPRER), but LYC alleviated these alterations. Therefore, LYC prevented DEHP-induced hepatic mitochondrial dynamics and MAM disorder, leading to ER stress. The present study provides novel evidence of mitochondria-ER coupling as a target for LYC that prevents DEHP-induced hepatotoxicity.
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