Coffea arabica pulp aqueous extract attenuates oxidative stress and hepatic lipid accumulation in HepG2 cells

Abstract

Coffea arabica pulp aqueous extract (CPE) contains several bioactive compounds including chlorogenic acid (CGA), caffeine, catechin and epicatechin. These constituents exhibit several biological activities including antibacterial, anti-inflammatory, antioxidant, and lipid-lowering activities. Therefore, it was hypothesized that polyphenol-rich CPE could exert hepatic lipid-lowering effects on a human hepatocyte cell line. The present study investigated the effect of CPE against oxidative stress and hepatic lipid accumulation in hepatocellular carcinoma (HepG2) cells. The major constituents in CPE were identified using nuclear magnetic resonance imaging, and the effect of CPE and its major constituents, CGA and caffeine, on intracellular oxidative stress and hepatic lipid accumulation were quantified using fluorescent 2',7'-dichlorodihydrofluorescein diacetate (H2DCFDA) and Nile red staining followed by flow cytometry. Total triglyceride (TG) and cholesterol (TC) contents and secretion were determined. Genes involving hepatic lipid metabolism and transporters were evaluated using real-time PCR. CPE and CGA exhibited antioxidant capacity against ABTS+, DPPH and hydrogen peroxide-induced oxidative stress without any cytotoxic effects in HepG2 cells. Intracellular lipid contents, TG and TC, were decreased and correlated with cholesterol secretion by CGA, caffeine and CPE. These findings were related mainly through downregulating peroxisome proliferator-activated receptor γ (PPAR γ), a lipogenic gene, and upregulating PPARα, a lipolytic gene. Correspondingly, CPE increased cholesterol efflux transporter ABCG5/8, decreased free fatty acid (FFA) uptake transporter fatty acid translocase (FAT/CD36) and strongly alleviated FFA-induced hepatic lipid accumulation. Taken together, CPE has effective antioxidant and hepatic lipid-lowering effects and could potentially be developed as a nutraceutical product to prevent dyslipidaemia-induced hepatic steatosis.