Herbal SGR Formula Prevents Acute Ethanol-Induced Liver Steatosis via Inhibition of Lipogenesis and Enhancement Fatty Acid Oxidation in Mice

Abstract

Our previous study indicated that herbal SGR formula partially attenuates ethanol-induced fatty liver, but the underlying mechanisms remain unclear. In the present study, mice were pretreated with SGR (100 and 200 mg/kg/d bw) for 30 d before being exposed to ethanol (4.8 g/kg bw). The biochemical indices and histopathological changes were examined to evaluate the protective effects and to explore potential mechanisms by investigating the adiponectin, tumor necrosis factor-α (TNF-α), peroxisome proliferators-activated receptor-α (PPAR-α), sterol regulatory element binding protein-1c (SREBP-1c), adenosine monophosphate-activated protein kinase (AMPK), and so forth. Results showed that SGR pretreatment markedly inhibited acute ethanol-induced liver steatosis, significantly reduced serum and hepatic triglyceride (TG) level, and improved classic histopathological changes. SGR suppressed the protein expression of hepatic SREBP-1c and TNF-α and increased adiponectin, PPAR-α, and AMPK phosphorylation in the liver. Meanwhile, acute toxicity tests showed that no death or toxic side effects within 14 days were observed upon oral administration of the extracts at a dose of 16 g/kg body wt. These results demonstrate that SGR could protect against acute alcohol-induced liver steatosis without any toxic side effects. Therefore, our studies provide novel molecular insights into the hepatoprotective effect of SGR formula, which may be exploited as a therapeutic agent for ethanol-induced hepatosteatosis.

Small heterodimer partner deficiency exacerbates binge drinking‑induced liver injury via modulation of natural killer T cell and neutrophil infiltration

“…In the current acute alcohol binge administration study, the degrees of hepatic lipid accumulation and lipid peroxidation did not vary between WT and SHP-KO mice. Previous studies have demonstrated that chronic and acute alcohol-induced steatosis may share a common mechanism responsible for the upregulation of lipid biosynthesis and lipid oxidation, which involves sterol regulatory element-binding protein 1 in fatty acid synthesis and AMP-dependent protein kinase, peroxisome proliferator-activated receptor (PPAR)α and adiponectin in lipid oxidation ( 33 , 38 – 40 ). To the best of our knowledge, although the underlying mechanisms responsible for the phenotypic differences resulting from alcohol-associated hepatic steatosis are largely undetermined, based on the inconsistent degrees of hepatic lipid accumulation between acute and chronic alcohol administered SHP-KO mice, it may be hypothesized that the role of SHP in hepatic lipid metabolism may vary between acute and chronic alcohol ingestion conditions.…”

Protective effects ofGinkgo bilobaL. against natural toxins, chemical toxicities, and radiation: A comprehensive review

“…In another research, Qiu et al () investigated the effects of a triple mixed herbal formulation named SGR on fatty liver developed by chronic ethanol consumption. This formulation consists of three herbs: Semen Hoveniae extract: 80%, GBLE: 10%, and Rosa roxburghii Tratt extract: 10%.…”

“…Findings of this study represented that ethanol elevated the triglyceride level in serum and liver tissue of mice through the decreased expression level of adiponectin, peroxisome proliferator‐activated receptor (PPAR‐α) and AMPK‐β, and increased expression level of TNF‐α and sterol regulatory element binding protein 1c (SREBP‐1c). SGR administration for 30 days had the potential of regulating the expression of adiponectin, PPAR‐α, TNF‐α, SREBP‐1c, and the level of phosphorylated AMPK‐β, instead of the total expression of AMPK‐β (Qiu et al, ). In the studies, which are conducted on a combination of several herbs, there is an uncertainty in making conclusion about the effects of every herbal component, unless some treated groups with the isolated or purified herbal extracts are added.…”

“…It was clarified that CO inhibited the ethanol-induced CYP 2 E 1 up-regulation, an enzyme involved in oxidative stress. Therefore, quercetin can attenuate the oxidative damages of ethanol through the up-regulation of HO-1 and then its metabolite, CO(Yao et al, 2009).In another research,Qiu et al (2015) investigated the effects of a triple mixed herbal formulation named SGR on fatty liver developed by chronic ethanol consumption. This formulation consists of three herbs: Semen Hoveniae extract: 80%, GBLE: 10%, and Rosa roxburghii Tratt extract: 10%.…”

Selenite supplementation modulates the hepatic metabolic sensors AMPK and SIRT1 in binge drinking exposed adolescent rats by avoiding oxidative stress

“…Alcohol, even in the form of BD, is known to affect SIRT1 as it decreases the NAD+/NADH ratio, on which SIRT1 is dependent 16 . On the other hand, different works establish that alcohol decreases the phosphorylation and activation of AMPK [17][18][19][20] . It seems that during the oxidation of NADH, produced by the metabolism of alcohol, energy generated is used to synthesize ATP; therefore, the AMP/ATP ratio is decreased and AMPK inhibited 21 .…”