The Effect of Inflammatory Cytokines in Alcoholic Liver Disease

Kawaratani, Hideto; Tsujimoto, Tatsuhiro; Douhara, Akitoshi; Takaya, Hiroaki; Moriya, Kyoji; Namisaki, Tadashi; Noguchi, Ryuichi; Yoshiji, Hitoshi; Fujimoto, Masao; Fukui, Hiroshi

doi:10.1155/2013/495156

Cited by 188 publications

(124 citation statements)

References 111 publications

(108 reference statements)

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“…All these factors act in concert to exacerbate the liver damage such as hepatitis, hepatic steatosis, and hepatocirrhosis. 38,39 LC27 or/and LC67 significantly reduced the ethanol-induced ALT and AST levels in the blood, which are one of the most widely used means for assessing the extent of hepatic damage, 40 as well as the TG and TC levels in the liver and blood. LC67 more potently reduced the ALT and AST levels.…”

Section: Discussionmentioning

confidence: 99%

Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 mitigate alcoholic steatosis in mice by inhibiting LPS-mediated NF-κB activation through restoration of the disturbed gut microbiota

Kim

Kwon

et al. 2018

Food Funct.

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Long-term exposure to ethanol simultaneously causes gastrointestinal inflammation, liver injury, and steatosis. In the present study, we investigated the effects of Bifidobacterium longum LC67, Lactobacillus plantarum LC27, and their mixture (LM) against ethanol-induced steatosis in mice. Exposure to ethanol caused liver damage: it increased ALT, AST, TG, TC, and lipopolysaccharide levels in the blood and induced NF-κB activation in the liver. Oral administration of LC27, LC67, or LM in mice reduced ethanolinduced ALT, AST, TG, and TC levels in the blood and liver. These also suppressed ethanol-induced NF-κB activation and α-smooth muscle actin expression in the liver and increased ethanol-suppressed AMPK activation. Treatment with LC27, LC67, or LM increased ethanol-suppressed alcohol dehydrogenase and acetaldehyde dehydrogenase activities in the liver, as well as tight junction protein expression in the liver and colon. Moreover, treatment with LC27, LC67, or LM restored the ethanol-disturbed gut microbiota composition, such as the increased population of Proteobacteria, and inhibited fecal and blood lipopolysaccharide levels. These inhibited NF-κB activation and increased tight junction protein expression in ethanol-or lipopolysaccharide-stimulated Caco-2 cells. These findings suggest that LC27, LC67, and LM can alleviate alcoholic steatosis by inhibiting LPS-mediated NF-κB activation through restoration of the disturbed gut microbiota.

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Section: Discussionmentioning

confidence: 99%

Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 mitigate alcoholic steatosis in mice by inhibiting LPS-mediated NF-κB activation through restoration of the disturbed gut microbiota

Kim

Kwon

et al. 2018

Food Funct.

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“…Thus, improvement of alcoholic liver injury has been proposed to be associated with inhibition of CYP2E1 (Lu & Cederbaum 2008). Moreover, it is well known that inflammatory cytokines, such as TNF-a, stimulate acute inflammation and are associated with the development liver injury in ALD, whereas hepatoprotective cytokines IL-6 is associated with attenuation of ALD (Kawaratani et al 2013). Thus, down-regulation of TNF-a and CYP2E1 can be therapeutic targets in ALD treatment (Schattenberg & Czaja 2014).…”

Section: Down-regulated Genes Expression Of Cyp2e1 and Inflammatory Cmentioning

confidence: 99%

Ligularia fischeriextract attenuates liver damage induced by chronic alcohol intake

Kim

Lee

et al. 2016

Pharmaceutical Biology

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Context Ligularia fischeri (Ledebour) Turcz. (Compositae) has been used as a leafy vegetable and in traditional medicine to treat hepatic disorder in East Asia. Objective The present study explores the antioxidant activity of LF aqueous extract on EtOHinduced oxidative stress accompanied by hepatotoxicity both in vitro and in vivo. Materials and methods In vitro study using the mouse liver NCTC-1469 cell line was conducted to estimate the cytotoxicity as well as the inhibitory effect of LF extract against alcohol-treated cell damage. In vivo study used an alcohol-fed Wister rat model orally administered EtOH (3.95 g/kg of body weight/d) with or without LF extract (100 or 200 mg/kg body weight) for 6 weeks. Serum and liver tissue were collected to evaluate hepatic injury and antioxidant-related enzyme activity. Results The EC 50 value for the DPPH radical scavenging capacity of LF extract was 451.5 mg/mL, whereas the IC 50 value of LF extract in terms of EtOH-induced reactive oxygen species (ROS) generation was 98.3 mg/mL without cell cytotoxicity. LF extract (200 mg/kg body weight) significantly reduced the triglyceride content of serum (33%) as well as hepatic lipid peroxidation (36%), whereas SOD activity was elevated three-fold. LF extract suppressed expression of CYP2E1 and TNF-a, and attenuated alcohol-induced abnormal morphological changes. Discussion and conclusion LF extract attenuated liver damage induced by alcoholic oxidative stress through inhibition of ROS generation, down-regulation of CYP2E1, and activation of hepatic antioxidative enzymes. Homeostasis of the antioxidative defence system in the liver by LF extract mitigated hepatic disorder following chronic alcohol intake. ARTICLE HISTORY

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“…Desde etapas tempranas, en la enfermedad hepática existe una acumulación masiva de lípidos en el hepatocito que inducen la liberación de diversos mediadores inflamatorios, entre los que se pueden mencionar la interleucina (IL) 1 y 6, el factor de necrosis tumoral (TNF) y la estimulación del receptor LPS/Toll-like (TLR-4) presentes en las células de Kupffer (14,15). Estas vías desencadenan una disregulación del endotelio mediante la activación de la dimetilarginina asimétrica (ADMA), un inhibidor endógeno de la óxido nítrico sintetasa (eNOS) (16,17).…”

Section: Alteraciones En La Hemostasia Primariaunclassified

Insuficiencia hepática crónica y hemostasia

Peñafiel

Sánchez

et al. 2017

Rev. Colomb. Gastroenterol.

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ResumenLa insuficiencia hepática es un estado patológico que condiciona la síntesis y metabolismo de diversas biomoléculas, siendo las alteraciones a la hemostasia una de las primeras consecuencias a nivel sistémico que se hacen presentes; debido a esto y por la dimensión de los riesgos de esta situación, no es raro que las pruebas de coagulación sean indispensables para formular las escalas pronósticas en pacientes hepatópatas.Los conocimientos sobre hemostasia han avanzado en la última década; la clásica cascada de activación de los factores de la coagulación ha sido perfeccionada hasta conformarse el ahora vigente modelo celular que considera la valiosa e indispensable participación del endotelio y las plaquetas. Gracias a esto es posible comprender que, en pacientes con insuficiencia hepática, el riesgo de sangrado no obedece únicamente a la deficiencia en la producción de los factores de la coagulación y, por tanto, es cuestionable la administración de vitamina K. Más relevante aún es que, gracias a estos conocimientos, se puede comprender el a veces contradictorio riesgo de trombosis en estos pacientes, complicación potencialmente mortal. Palabras claveCoagulación sanguínea, insuficiencia hepática, trombosis, vitamina K. AbstractHepatic insufficiency is a pathology that conditions synthesis and metabolism of various biomolecules. Alterations of hemostasis is one of its first systemic consequences. Because of this and the size of the risks, it is not uncommon for clotting tests to be indispensable for formulating prognostic scales in patients with liver disease.Knowledge about hemostasis has advanced in the last decade, and the classic cascade of activation of coagulation factors has been perfected until it has become the now-current cellular model that considers the valuable and indispensable participation of the endothelium and platelets. Thanks to this, it is possible to understand that the risk of bleeding in patients who have hepatic insufficiency is not only due to deficiencies in production of coagulation factors, and that for this reason administration of vitamin K is questionable. Even more relevant, is the fact that, thanks to this this knowledge, we can understand the sometimes contradictory and potentially life-threatening complication of thrombosis in these patients.

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The Effect of Inflammatory Cytokines in Alcoholic Liver Disease

Cited by 188 publications

References 111 publications

Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 mitigate alcoholic steatosis in mice by inhibiting LPS-mediated NF-κB activation through restoration of the disturbed gut microbiota

Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 mitigate alcoholic steatosis in mice by inhibiting LPS-mediated NF-κB activation through restoration of the disturbed gut microbiota

Ligularia fischeriextract attenuates liver damage induced by chronic alcohol intake

Insuficiencia hepática crónica y hemostasia

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