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Life sciences

Epigallocatechin-3-gallate protects against 1,3-dichloro-2-propanol-induced lipid accumulation in C57BL/6J mice.


PMID 30092300

Abstract

Chloropropanol is a contaminant produced during food processing, and 1,3-dichloro-2-propanol (1,3-DCP) is one of the most-studied and most common chloropropanol-related food contaminants. Epigallocatechin-3-gallate (EGCG) is the most abundant ester catechin in tea polyphenols. We studied the potential therapeutic effect of EGCG on 1,3-DCP-induced lipid accumulation in the liver of mice, and determined the related regulatory mechanisms. The effects of EGCG were investigated in 6-8-week-old adult male C57BL/6J mice that were given 1,3-DCP (1 mg/kg bw/day; i.g.) for 6 weeks. EGCG (10, 31.6 and 100 mg/kg bw/day i.g.) was administered daily in the 1,3-DCP-treated mice for 10 days. Total cholesterol (TC) and triglyceride (TG) were measured in serum and liver. For histological examination, HE staining and oil red O experiments were performed. Western blot and quantitative RT-PCR were subsequently used to study the molecular mechanisms. Increasing concentrations of EGCG significantly lowered TC and TG levels compared with those of the model group. Furthermore, EGCG dramatically increased expression of cAMP, P-PKA and P-CREBP, -AMPKα (Tr172), LKB1, P-ACC (Ser79) and lowered expression of CD36, SREBP-2, HMGCR, SREBP-1, GPAT in 1,3-DCP-treated mice livers. Quantitative RT-PCR experiments showed that EGCG regulated gene transcription of AMPK, SREBF-2, HMGCR and SREBP-1c. These data suggested that EGCG intervention restored 1,3-DCP-altered protein levels and reduced hepatic lipid levels to normal. The mechanism was mediated by the AMPK and PKA pathways. EGCG may be developed as a candidate natural agent for the treatment of 1,3-DCP-induced lipid accumulation.