期刊
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
卷 63, 期 22, 页码 5468-5475出版社
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.5b01750
关键词
NHDC; Keap1; HO-1; NQO1; MAPK; liver; ubiquitination
资金
- National Natural Science Foundation of China [21477098]
- Science and Technology Talent Cultivation Project of Chongqing [cstc2014kjrc-qnrc00001]
- Fundamental Research Funds for the Central Universities [XDJK2014A020, XDJK2015A017]
Neohesperidin dihydrochalcone (NHDC), a sweetener derived from citrus, belongs to the family of bycyclic flavonoids dihydrochalcones. NHDC has been reported to act against CCl4-induced hepatic injury, but its mechanism is still unclear. We first discovered that NHDC showed a strong ability to scavenge free radicals. In addition, NHDC induces the phase II antioxidant enzymes heme oxygenase 1 (HO-1) and NAD(P)H/quinone oxidoreductase 1 (NQO1) through the activation of the nuclear factor (erythroid-derived 2)-like 2 (Nrf2)/antioxidant response element (ARE) signaling. Further assays demonstrated that NHDC induces accumulation of Nrf2 in the nucleus and augmented Nrf2-ARE binding activity. Moreover, NHDC inhibits the ubiquitination of Nrf2 and suggests the modification of Kelch-like ECH-associated protein 1 (Keap1) and the disruption of the Keap1/Nrf2 complex. c-Jun N-terminal kinase (JNK) and p38 but not extracellular signal-regulated protein kinase (ERK) phosphorylations were up-regulated by NHDC treatment. Taken together, NHDC showed its protective antioxidant effect against CCl4-induced oxidative damage via the direct free radical scavenging and indirect Nrf2/ARE signaling pathway.
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