期刊
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 68, 期 41, 页码 11468-11479出版社
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.0c05077
关键词
di(2-ethylhexyl) phthalate; lycopene; lipid metabolism; hypoxia-inducible factor-1 alpha
资金
- National Natural Science Foundation of China [31572586]
- Excellent Youth Foundation of Heilongjiang Province of China [JC2017005]
- China Agriculture Research System [CARS-35]
Di(2-ethylhexyl) phthalate (DEHP) is a widespread pollutant that badly affects animals and human health. Lycopene (LYC) has been used as a dietary supplement that has effective antioxidant and antiobesity functions. The present goal was to understand the molecular mechanisms of LYC preventing DEHP-induced lipid metabolism of the liver. The mice were intragastrically administered with LYC (5 mg/kg) and/or DEHP (500 mg/kg or 1000 mg/kg). Here, we found that LYC attenuated DEHP-caused hepatic histopathological lesions including steatosis. Hematological and biochemical analyses revealed that LYC ameliorated DEHP-caused liver function and lipid metabolism disorders. DEHP caused lipid metabolism disorders via activating the peroxisome proliferator activated receptor alpha/gamma (PPAR alpha/gamma) signal transducer and Farnesoid X receptor (FXR)/liver X receptor (LXR) signaling pathway. As a major regulator of lipid metabolism, hypoxia-inducible factor-1 alpha (HIF-1 alpha) system was elevated with increased fatty degeneration under DEHP exposure. However, LYC could decrease the levels of HIF-1 alpha/PPAR alpha/PPAR gamma/FXR/LXR signaling pathway-related factors. Our research indicated that LYC could prevent DEHP-induced lipid metabolism disorders via inhibiting the HIF-1 alpha-mediated PPAR alpha/PPAR gamma/FXR/LXR system. This study may provide a possible molecular mechanism for fatty liver induced by DEHP.
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