Ecklonia cava polyphenol protects the liver against ethanol-induced injury in rats

Takahashi, Masakazu; Satake, Naoko; Yamashita, Haruka; Tamura, Akiko; Sasaki, Mio; Matsui‐Yuasa, Isao; Tabuchi, Masaki; Akahoshi, Yasumitsu; Terada, Masaki; Kojima‐Yuasa, Akiko

doi:10.1016/j.bbagen.2012.02.008

Cited by 25 publications

(23 citation statements)

References 41 publications

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“…It has been reported that hepatic histological changes in ethanol-induced fibrosis model were similar to those found in human alcoholic cirrhosis. 24) Many studies have confirmed that the reduction in body weight was related to the toxicity of the ethanol because ethanol impaired the activation and utilization of nutrients due to maldigestion or malabsorption, 25) while increased liver weight could be due to accumulation of lipids and collagen. 26) In the present study, combination drugs could markedly improve animal diet and activity, reduce death ratio, increase body weight, and decrease the liver index compared with that in model group, which indicated that combination drugs could efficiently repair the injury originated from alcohol and retrieve nutrients leading to the improved vital signs.…”

Section: Discussionmentioning

confidence: 99%

Combination Therapy with Taurine, Epigallocatechin Gallate and Genistein for Protection against Hepatic Fibrosis Induced by Alcohol in Rats

Zhuo

Liao

et al. 2012

Biological & Pharmaceutical Bulletin

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This study was to investigate the possibility of enhancing the anti-fibrotic effect by using a combination therapy with taurine, epigallocatechin gallate and genistein in a rat liver fibrosis model induced by alcohol, and to explore its underlying mechanism. Hepatic fibrosis was induced by intragastric administration with various amount of alcohol (5.0-9.5 g/kg) within 24 weeks in rats. The model group received alcohol only, and treatment groups received the corresponding drugs plus alcohol respectively, while the normal control group received an equal volume of saline. The antifibrotic effects of combination therapy were assessed directly by hepatic histology, and indirectly by measurement of serum biochemical markers, the fibrosis markers and related key cytokines/proteins. The results showed that combination therapy could significantly improve the liver function, as indicated by decreasing levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, γ-glutamyltransferase, interleukin-6 and tumor necrosis factor-α. Moreover, combination therapy could effectively suppress the serum levels of fibrosis markers and hepatic hydroxyproline content, inhibit collagen deposition and reduce the pathological tissue damage. Research on mechanism showed that combination therapy was able to markedly reduce lipid peroxidation and recruit the anti-oxidative defense system, and inhibit the expression of B-cell lymphoma 2, α-smooth muscle actin, transforming growth factor β 1 and small mothers against decapentaplegic homolog 3 proteins. Our results showed that combination therapy is effective in attenuating hepatic injury and fibrosis in the alcohol-induced rat model. The improved efficacy of the combination therapy with its good safety profile could represent a new protective approach for liver fibrosis.

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Section: Discussionmentioning

confidence: 99%

Combination Therapy with Taurine, Epigallocatechin Gallate and Genistein for Protection against Hepatic Fibrosis Induced by Alcohol in Rats

Zhuo

Liao

et al. 2012

Biological & Pharmaceutical Bulletin

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“…Several methods of alcohol administration have been used extensively in rodent models to study the mechanisms of alcoholic liver, lung, and cardiovascular disease including the Lieber‐DeCarli liquid ethanol (EtOH) diet, Tsukamoto‐French intragastric feeding model, EtOH in the drinking water, and more recently, the National Institute on Alcohol Abuse and Alcoholism model, which combines chronic‐plus‐binge alcohol feeding to more closely mimic the drinking patterns of patients that develop alcoholic hepatitis (Bertola et al., ; Crestani et al., ; Kaphalia et al., ; Mathews et al., ; Romero et al., ; Takahashi et al., ). Although these classic models have been able to successfully produce peripheral tissue injury, they have several drawbacks.…”

mentioning

confidence: 99%

Alcohol Vapor Inhalation as a Model of Alcohol‐Induced Organ Disease

Mouton

Maxi

Souza‐Smith

et al. 2016

Alcoholism Clin & Exp Res

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Background Chronic intermittent ethanol vapor exposure (CIEV) has been used extensively to produce rodent models of alcohol dependence, but unlike other models of alcohol abuse, CIEV has not been assessed as a model of end-organ damage. The purpose of this study was to characterize the effects of CIEV on peripheral organ systems affected by alcohol abuse, including the liver, lungs and cardiovascular system. Methods Adult male Sprague-Dawley rats were exposed to daily CIEV for a period of 8 weeks (14HR ON/10HR OFF), producing blood alcohol levels of ~200 mg/dl. Controls were exposed to room air. After 8-weeks, echocardiography was performed to assess cardiac function. Indices of liver injury (alanine and aspartate aminotransferases (ALT and AST); cytochrome p450 2E1 (CYP2E1); alcohol dehydrogenase (ADH); Oil Red-O and triglyceride content; lipid peroxidation; inflammatory cytokine expression and macrophage infiltration), and lung inflammatory cell count, proinflammatory cytokine expression, and lipid peroxidation were measured. Results Left ventricular posterior wall thickness was significantly decreased, and systolic blood pressure was significantly elevated by CIEV compared to air controls. CIEV led to a significant increase in plasma ALT and triglycerides compared to room air controls. CIEV did not affect liver triglyceride content, lipid staining or peroxidation, but increased CYP2E1 and CCL2 protein expression, while decreasing ADH expression. CIEV significantly increased numbers of both PMNs and lymphocytes in the BALF, indicative of pulmonary inflammation. However, CIEV did not produce significant changes in lung mass, pulmonary lipid peroxidation, inflammatory cytokine expression, or edema. Conclusions These results show that CIEV produces hepatic, pulmonary and cardiovascular effects in rats similar to those found in other models of chronic alcohol administration. Alcohol vapor administration is a novel method of alcohol-induced tissue injury with high potential for widespread use in alcohol toxicology research.

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“…We previously demonstrated that a treatment of 100 mM ethanol for 24 h significantly decreased cell viability of hepatocytes compared with control cells [15]. Here, we measured the cell viability of hepatocytes treated with 100 mM ethanol with or without various concentrations of DNSM.…”

Section: Resultsmentioning

confidence: 99%

“…Contrastingly, Siegers et al developed a model for the administration of low-dose carbon tetrachloride (CCl 4 ) and a 5% ethanol solution that produced histological changes in rats similar to those found in human alcoholic cirrhosis within four weeks [14]. We have also shown that hepatic histological changes occurred within four weeks of the administration of low-dose CCl 4 and a 5% ethanol solution [15,16]. …”

Section: Introductionmentioning

confidence: 87%

Protective Effects of Hydrolyzed Nucleoproteins from Salmon Milt against Ethanol-Induced Liver Injury in Rats

et al. 2016

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Dietary nucleotides play a role in maintaining the immune responses of both animals and humans. Oral administration of nucleic acids from salmon milt have physiological functions in the cellular metabolism, proliferation, differentiation, and apoptosis of human small intestinal epithelial cells. In this study, we examined the effects of DNA-rich nucleic acids prepared from salmon milt (DNSM) on the development of liver fibrosis in an in vivo ethanol-carbon tetrachloride cirrhosis model. Plasma aspartate transaminase and alanine transaminase were significantly less active in the DNSM-treated group than in the ethanol plus carbon tetrachloride (CCl4)-treated group. Collagen accumulation in the liver and hepatic necrosis were observed histologically in ethanol plus CCl4-treated rats; however, DNSM-treatment fully protected rats against ethanol plus CCl4-induced liver fibrosis and necrosis. Furthermore, we examined whether DNSM had a preventive effect against alcohol-induced liver injury by regulating the cytochrome p450 2E1 (CYP2E1)-mediated oxidative stress pathway in an in vivo model. In this model, CYP2E1 activity in ethanol plus CCl4-treated rats increased significantly, but DNSM-treatment suppressed the enzyme’s activity and reduced intracellular thiobarbituric acid reactive substances (TBARS) levels. Furthermore, the hepatocytes treated with 100 mM ethanol induced an increase in cell death and were not restored to the control levels when treated with DNSM, suggesting that digestive products of DNSM are effective for the prevention of alcohol-induced liver injury. Deoxyadenosine suppressed the ethanol-induced increase in cell death and increased the activity of alcohol dehydrogenase. These results suggest that DNSM treatment represents a novel tool for the prevention of alcohol-induced liver injury.

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Ecklonia cava polyphenol protects the liver against ethanol-induced injury in rats

Cited by 25 publications

References 41 publications

Combination Therapy with Taurine, Epigallocatechin Gallate and Genistein for Protection against Hepatic Fibrosis Induced by Alcohol in Rats

Combination Therapy with Taurine, Epigallocatechin Gallate and Genistein for Protection against Hepatic Fibrosis Induced by Alcohol in Rats

Alcohol Vapor Inhalation as a Model of Alcohol‐Induced Organ Disease

Protective Effects of Hydrolyzed Nucleoproteins from Salmon Milt against Ethanol-Induced Liver Injury in Rats

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