Inhibitory Effect of Blueberry Polyphenolic Compounds on Oleic Acid-Induced Hepatic Steatosis in Vitro

Abstract

Nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver diseases worldwide and is closely associated with metabolic syndromes, such as obesity, diabetes, and insulin resistance. Nonalcoholic fatty liver (NAFL), also called simple steatosis, is the initial phase of NAFLD, which is accompanied the characteristic pathological overaccumulation of lipids without inflammation. To prevent NAFLD from reaching the NAFL stage through dietary therapy, in the present work, wild Chinese blueberries (Vacciniun spp.) were selected for their well-known benefits in inhibiting metabolic syndrome. After being purified from wild Chinese blueberries, polyphenol-rich extracts were subsequently separated into three fractions, namely, anthocyanin-rich fraction, phenolic acid-rich fraction, and ethyl acetate extract. The inhibition of oleic acid (OA)-induced triglyceride (TG) deposition in HepG 2 cells was referred to as the potential activity of preventing NAFL. Biochemical indicators, such as cytotoxicity, TG level, levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and intracellular reactive oxygen species, were used to evaluate the analogous pathological stage of NAFLD. The results show that OA ≤ 1.0 mM exhibits a dose-dependent induction of TG accumulation, and no inflammation was observed based on the changes in ALT and AST levels. Therefore, 1.0 mM OA was used to simulate an in vitro fatty liver. Blueberry polyphenol-rich extract efficiently inhibited OA-induced TG accumulation in HepG2 cells, and the phenolic acid-rich fraction performed efficiently. Seven phenolic acids were subsequently identified using a high-performance liquid chromatography assay, and the main types were caffeic, chlorogenic, ferulic, p-coumaric, and cinnamic acids. These phenolic acid standards also displayed good efficiency in inhibiting TG accumulation in HepG2 cells. These results imply that wild Chinese blueberries have a potential preventive effect on NAFLD in its early stage, and phenolic acids are the most efficient component.

Persimmon tannin alleviates hepatic steatosis in L02 cells by targeting miR-122 and miR-33b and its effects closely associated with the A type ECG dimer and EGCG dimer structural units

“…A number of studies suggested that condensed tannins (proanthocyanidins) could improve metabolic syndrome such as dyslipidemia (Hsu & Yen, 2007;Liu et al, 2011), atherosclerosis (Zang et al, 2006), and non-alcoholic steatohepatitis (Kuzu et al, 2008). Our previous study showed that persimmon tannin could prevent hepatic steatosis in high-fat induced rats, and it was the main active component being responsible for the anti-hyperlipidemic effect of persimmon extract (Zou et al, 2014).…”

A-type ECG and EGCG dimers disturb the structure of 3T3-L1 cell membrane and strongly inhibit its differentiation by targeting peroxisome proliferator-activated receptor γ with miR-27 involved mechanism

“…Dietary polyphenols attracted many scientists' attention due to their significant effects on improving metabolic syndrome such as dyslipidemia [7,8], atherosclerosis [9], and non-alcoholic steatohepatitis [10][11]. Monomeric polyphenols such as apigenin [12] and epigallocatechin-3-O-gallate (EGCG) [13], resveratrol [14], curcumin [15], and polyphenolic extracts such as cocoa polyphenols extract and grape seed extract [3,16] were reported to inhibit 3T3-L1 adipocyte differentiation effectively through the suppression of PPARγ.…”

Prunus mume Sieb. et Zucc. fruit ameliorates alcoholic liver injury in mice by inhibiting apoptosis and inflammation through oxidative stress

“…Natural antioxidants have received attention as therapeutic agents for the prevention or treatment of alcohol-induced liver injury (Hou, Qin, & Ren, 2010;Kaviarasan, Sundarapandiyan, & Anuradha, 2008;Liu et al, 2011;Nanji et al, 2003). Although PME is a promising antioxidant source, there is little evidence available regarding the molecular mechanisms underlying the efficacy of PME in alcoholic liver injury.…”