<p>Galangin Improved Non-Alcoholic Fatty Liver Disease in Mice by Promoting Autophagy</p>

Abstract

Background: Previous studies have shown that curcumin derivatives can improve the fatty degeneration of liver tissue that occurs in nonalcoholic fatty liver disease (NAFLD). However, the specific mechanism for that improvement remains unclear. We examined whether the curcumin derivative galangin could reduce the fatty degeneration of liver tissue in mice with NAFLD by inducing autophagy, from the perspective of both prevention and treatment. Methods: C57BL/6J mice were randomly assigned to a prevention group (given galangin and a HFD simultaneously) or a treatment group (given galangin after being fed an HFD). The prevention group was treated with galangin (100 mg/kg/d) or an equal volume of normal saline (NS) while being fed an HFD. Some mice were treated with an autophagy inhibitor (3-methyladenine, 3-MA; 30 mg/kg/biwk, i.p.) while being fed an HFD and galangin. HepG2 cells were cultured in DMEM medium containing both free fatty acids and galangin. Results: Galangin was found to reduce the fatty degeneration of liver tissue induced by eating an HFD at both the prevention and treatment levels, and that effect might be related to an enhancement of hepatocyte autophagy. Inhibition of autophagy by 3-MA blocked the protective effect of galangin on hepatic steatosis. At the cellular level, galangin reduced lipid accumulation and enhanced the level of hepatocyte autophagy. Conclusion: In vitro and in vivo studies showed that galangin cannot only improve preexisting hepatic steatosis but also prevent the development of stenosis by promoting hepatocyte autophagy.

Protective effects of propolis on hepatic steatosis and fibrosis among patients with nonalcoholic fatty liver disease (NAFLD) evaluated by real‐time two‐dimensional shear wave elastography: A randomized clinical trial

“…Galangin which is one of the polyphenols in poplar propolis suppresses hepatic inflammation and oxidative damage through the activation of nuclear factor erythroid 2‐related factor 2 (Nrf‐2) (Sanyal et al, 2010). Prior studies showed that galangin not only attenuates hepatic steatosis via promoting hepatocyte autophagy (Zhang et al, 2020), but also inhibits HSCs proliferation and collagen gene expression via inhibiting TGF‐β expression (Wang et al, 2013). Propolin G is another polyphenols in propolis that were shown to down‐regulate collagen gene expression through eliminating JNK and TGF‐β/Smad signaling pathways, stimulating apoptosis‐related protein expression, and inhibiting proliferation in the HSCs treated with TGF‐β (Su et al, 2014).…”

“…Galangin which is one of the polyphenols in poplar propolis suppresses hepatic inflammation and oxidative damage through the activation of nuclear factor erythroid 2-related factor 2 (Nrf-2) (Sanyal et al, 2010). Prior studies showed that galangin not only attenuates hepatic steatosis via promoting hepatocyte autophagy (Zhang et al, 2020), but also inhibits HSCs proliferation and collagen gene expression via inhibiting TGF-β expression (Wang et al, 2013).…”

Autophagy: A Cellular Guardian against Hepatic Lipotoxicity

“…ω-3 fatty acids present in fish oil, flaxseeds, and walnuts prevent FFA-induced lipotoxicity through induction of autophagy in NAFLD [ 105 ]. Similarly, widely used components in Indian traditional medicine, curcumin and its derivatives have shown protective effects in animal models of NAFLD by an autophagy-mediated pathway [ 106 ].…”

Galangin: A food‐derived flavonoid with therapeutic potential against a wide spectrum of diseases

“…Zhang et al reported that galangin alleviated hepatic steatosis through regulating the expressions of becline1, LC3-II/LC3-I, Atg3, AMPKα1, and decreased mTOR protein expression to promote hepatocyte autophagy in NAFLD mice (Zhang et al, 2020).…”