Effects of antrosterol from Antrodia camphorata submerged whole broth on lipid homeostasis, antioxidation, alcohol clearance, and anti-inflammation in livers of chronic-alcohol fed mice

Chang, Yuan Yen; Liu, Yichen; Kuo, Yueh‐Hsiung; Lin, Yi-Ling; Wu, Yi-Hsieng Samuel; Chen, Jr-Wei; Chen, Yi‐Chen

doi:10.1016/j.jep.2017.03.003

Cited by 28 publications

(29 citation statements)

References 26 publications

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“…Along with the promoted inflammatory response, the levels of liver fibrosis markers, such as α-SMA, collagens and TIMP-1, were elevated in alcohol-fed mice. In addition, with increasing collagen deposition, our data indicated that mild liver fibrosis might have occurred in mice fed with a Lieber-DeCarli ethanol liquid diet for 4 weeks, which was similar to a previous report (Chang et al, 2017). With GPS administration, those liver fibrosis marker levels were restored to normal levels, suggesting GPS might possess the ability to restrain the progression from alcoholic hepatic steatosis to hepatic fibrosis.…”

Section: Discussionsupporting

confidence: 90%

“…All histograms represent the mean ± SD of at least three independent assays. diet containing 5% (v/v) alcohol, proteins related to liver fibrosis were upregulated (Chang et al, 2017). Masson trichrome staining data of mouse livers showed that mice exposed to chronic and excessive alcohol exhibited increased collagen deposition, indicating that excessive alcohol consumption might induce a mild fibrosis in mouse livers (Fig.…”

Section: Gps Reversed Ecm Deposition In Chronic Alcohol Intakeinducedmentioning

confidence: 91%

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Gentiopicroside Ameliorates the Progression from Hepatic Steatosis to Fibrosis Induced by Chronic Alcohol Intake

Yang

Shang

Jin

et al. 2020

Biomolecules & Therapeutics

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In current study, we aimed to investigate whether the gentiopicroside (GPS) derived from Gentiana manshurica Kitagawa could block the progression of alcoholic hepatic steatosis to fibrosis induced by chronic ethanol intake. C57BL/6 mice were fed an ethanol-containing Lieber-DeCarli diet for 4 weeks. LX-2 human hepatic stellate cells were treated with GPS 1 h prior to transforming growth factor-β (TGF-β) stimulation, and murine hepatocyte AML12 cells were pretreated by GPS 1 h prior to ethanol treatment. GPS inhibited the expression of type I collagen (collagen I), α-smooth muscle actin (α-SMA) and tissue inhibitor of metal protease 1 in ethanol-fed mouse livers with mild fibrosis. In addition, the imbalanced lipid metabolism induced by chronic ethanol-feeding was ameliorated by GPS pretreatment, characterized by the modulation of lipid accumulation. Consistently, GPS inhibited the expression of collagen I and α-SMA in LX-2 cells stimulated by TGF-β. Inhibition of lipid synthesis and promotion of oxidation by GPS were also confirmed in ethanol-treated AML12 cells. GPS could prevent hepatic steatosis advancing to the inception of a mild fibrosis caused by chronic alcohol exposure, suggesting GPS might be a promising therapy for targeting the early stage of alcoholic liver disease.

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Section: Discussionsupporting

confidence: 90%

Section: Gps Reversed Ecm Deposition In Chronic Alcohol Intakeinducedmentioning

confidence: 91%

Gentiopicroside Ameliorates the Progression from Hepatic Steatosis to Fibrosis Induced by Chronic Alcohol Intake

Yang

Shang

Jin

et al. 2020

Biomolecules & Therapeutics

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“…Increased de novo lipogenesis is one of stimuli for alcohol‐induced steatosis . The change in NADH:NAD + ratio in alcohol catabolism upregulates SREBP1c, thus triggering de novo lipogenesis.…”

Section: Resultsmentioning

confidence: 99%

“…However, excessive alcohol metabolism is always coupled with poisonous metabolites, i.e. ROS generation, imbalance of cellular energy metabolism and lipid aggregation, thus inducing steatohepatitis …”

Section: Introductionmentioning

confidence: 99%

Protective effects of antioxidant egg‐chalaza hydrolysates against chronic alcohol consumption‐induced liver steatosis in mice

Yang

Lin

et al. 2018

J Sci Food Agric

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BACKGROUND: Reactive oxygen species (ROS) overproduction is highly related to some human chronic diseases. There are approximately 400 metric tons of chalazae produced yearly after the processing of the liquid-egg production, which are disposed of as waste. The objectives of this study were to look for the optimal production condition of antioxidant crude chalaza hydrolysates and evaluate the in vivo antioxidant capacity via a chronic alcohol consumption mouse model. RESULTS: Antioxidant crude chalaza hydrolysates (CCH-As) could be produced by proteaseA at 1:100 ratio (w/w) and 0.5 h hydrolytic period. After our analyses, CCH-As were rich in leucine, arginine, phenylalanine, valine, lysine and antioxidant dipeptides (anserine and carnosine), and the major molecular masses were lower than 15 kDa. Regarding protective effects of CCH-As against oxidative damage in alcoholic-liquid-diet-fed mice, alcohol-fed mice had lower (P < 0.05) liver antioxidant capacities, and higher (P < 0.05) liver lipid contents, serum lipid/liver damage indices and IL-1 /IL-6 values. CCH-A supplementation reversed (P < 0.05) liver antioxidant capacities and reduced (P < 0.05) serum/liver lipids in alcohol-fed mice, which may result from increased (P < 0.05) fecal lipid output, upregulated (P < 0.05) fatty acid -oxidation and downregulated (P < 0.05) lipogenesis in the liver. CONCLUSION: Taken together, this CCH-A should benefit the liquid-egg industry, while also offering consumers a choice of healthy ingredients from animal sources.Keywords: alcoholic fatty liver; amino acid profile; in vitro and in vivo antioxidant effects; lipid metabolism; protease-A-digested crude chalaza hydrolysate Industry and 0.25 mL potassium ferricyanide (1%) (Sigma Co.), and the mixture was incubated at 50 ∘ C for 15 min. 0.25 mL trichloroacetic acid solution (10%) (Sigma Co.) was added to the mixture, which was then centrifuged at 900 × g for 10 min at room temperature. Then J Sci Food Agric 2019; 99: 2300-2310In vivo hepatoprotective effects of CCH-As Effects of CCH-As on body weight, size of organs and abdominal fat pad, serum biochemical values, liver damage status, and hepatic and fecal lipids in chronic alcohol-fed mice With regard to an in vivo antioxidant effect of our manufactured CCH-As, chronic alcoholic liquid-diet-fed mice were applied as J Sci Food Agric 2019; 99: 2300-2310

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“…And the main source of ROS in the liver is the cytochrome P45 enzymes [ 9 , 10 ]. CYP 2E1 is of great importance in alcohol-induced generation of oxidative stress, not only for its activity enhancement induced by alcohol, but also for its participation in alcohol metabolism [ 9 , 11 ]. Recently, it is reported that nuclear factor erythroid 2-related factor 2 (Nrf2) could protect against CYP2E1-induced oxidative stress through upregulation of antioxidant enzymes like HO-1 [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Polydatin Protects Rat Liver against Ethanol-Induced Injury: Involvement of CYP2E1/ROS/Nrf2 and TLR4/NF-κB p65 Pathway

Huang

Liu

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Excessive alcohol consumption leads to serious liver injury, associating with oxidative stress and inflammatory response. Previous study has demonstrated that polydatin (PD) exerted antioxidant and anti-inflammatory effects and attenuated ethanol-induced liver damage, but the research remained insufficient. Hence, this experiment aimed to evaluate the hepatoprotective effect and potential mechanisms of PD on ethanol-induced hepatotoxicity. Our results showed that PD pretreatment dramatically decreased the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) in the serum, suppressed the malonaldehyde (MDA) and triglyceride (TG) content and the production of reactive oxygen species (ROS), and enhanced the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), andalcohol dehydrogenase (ADH), and aldehyde dehydrogenase (ALDH), paralleled by an improvement of histopathology alterations. The protective effect of PD against oxidative stress was probably associated with downregulation of cytochrome P450 2E1 (CYP2E1) and upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its target gene haem oxygenase-1 (HO-1). Moreover, PD inhibited the release of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) via downregulating toll-like receptor 4 (TLR4) and nuclear factor kappa B (NF-κB) p65. To conclude, PD pretreatment protects against ethanol-induced liver injury via suppressing oxidative stress and inflammation.

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Effects of antrosterol from Antrodia camphorata submerged whole broth on lipid homeostasis, antioxidation, alcohol clearance, and anti-inflammation in livers of chronic-alcohol fed mice

Cited by 28 publications

References 26 publications

Gentiopicroside Ameliorates the Progression from Hepatic Steatosis to Fibrosis Induced by Chronic Alcohol Intake

Gentiopicroside Ameliorates the Progression from Hepatic Steatosis to Fibrosis Induced by Chronic Alcohol Intake

Protective effects of antioxidant egg‐chalaza hydrolysates against chronic alcohol consumption‐induced liver steatosis in mice

Polydatin Protects Rat Liver against Ethanol-Induced Injury: Involvement of CYP2E1/ROS/Nrf2 and TLR4/NF-κB p65 Pathway

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