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Objective It is known that alcoholic liver disease (ALD) caused by the acute and chronic exposure to alcohol is one of the chronic liver diseases with the high mortality. Sulforaphane (SFN), rich in various cruciferous vegetables, has been widely studied as a chemo-preventive agent. In this study, we focused on the protective effects of SFN on alcohol-induced toxicity and mechanisms.Methods Male C57BL/6 mice were orally administrated with SFN (0, 12, 40, 80 mg/ kg.bw) for 14 days. At the 13th day, mice were challenged with alcohol (5g/kg.bw) every 12 h for 3 times. Results SFN markedly reversed the alcohol induced decrease of antioxidant capacity through enhancing GSH, GSH-Px, GST redox system. And the protective actions are related with activating Nrf2 and inactivating NF-κB. SFN attenuated the triglyceride (TG) and cholesterol (CHOL) contents which is possibly mediated by down-regulating sterol regulatory element-binding protein-1 (SREBP-1c). In addition, SFN weakened the stimulation of the chaperone GRP78, and its downstream sensory receptor ATF-6, triggered by acute alcohol intake. Conclusion The results suggest that antioxygenation is involved in the protective effects of Sulforaphane on the alcohol-induced toxicity. The current findings indicated that SFN weakened the liver toxicity triggered by alcohol through enhancing antioxidant capacity and reducing the endoplasmic reticulum stress.

PROTECTIVE EFFECTS OF SULFORAPHANE ON THE ALCOHOL-INDUCED TOXICITY AND ENDOPLASMIC RETICULUM STRESS IN C57BL/6 MICE