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

Abstract:

AIMS: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. MATERIALS AND METHODS: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. KEY FINDINGS: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. SIGNIFICANCE: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.

journal_name

Life Sci

journal_title

Life sciences

authors

Lu J,Fang B,Huang Y,Tao S,Sun B,Guan S,Jin Y

doi

10.1016/j.lfs.2018.08.007

subject

Has Abstract

pub_date

2018-09-15 00:00:00

pages

324-331

eissn

0024-3205

issn

1879-0631

pii

S0024-3205(18)30454-5

journal_volume

209

pub_type

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