Alcoholic liver disease and the gut-liver axis

Szabó, Gyöngyi; Bala, Shashi

doi:10.3748/wjg.v16.i11.1321

Cited by 317 publications

(287 citation statements)

References 120 publications

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“…26) Furthermore, the major metabolic product of alcohol, that is, acetaldehyde, leads to serious consequences to the individual. Increasing and repeating acetaldehyde exposure from increased alcohol consumption can increase the risk of developing acetaldehyde-related pathologies in the patient; thus, acetaldehyde is more toxic to the body than alcohol.…”

Section: Discussionmentioning

confidence: 99%

Retraction: Asiatic Acid from Potentilla chinensis Attenuate Ethanol-Induced Hepatic Injury via Suppression of Oxidative Stress and Kupffer Cell Activation

Wei

Huang

et al. 2013

Biological & Pharmaceutical Bulletin

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This study examined the effect of Asiatic acid from Potentilla chinensis (AAPC) on chronic ethanolinduced hepatic injury. Rats underwent intragastric administration of ethanol (5.0-9.0 g/kg) once a day for 12 weeks. A subset of rats were also intragastrically treated with AAPC (2, 4 or 8 mg/kg) once a day. In the end, AAPC treatment significantly protected against ethanol-induced liver injury, as evidenced by the decrease in serum alanine and aspartate aminotransferases levels and the attenuation of histopathological changes in rats. Additionally, AAPC significantly decreased blood alcohol and acetaldehyde concentrations by enhancing alcohol dehydrogenase and aldehyde dehydrogenase activities. Mechanistically, studies showed that AAPC remarkably alleviated the formations of malondialdehyde and myeloperoxidase, restored impaired antioxidants, including superoxide dismutase, glutathione peroxidase, glutathione reductase and catalase, and inhibited cytochrome P450 (CYP)2E1 activity. Moreover, the over-expression of cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), the elevated plasma endotoxin level and the up-regulated Toll-like receptor 4 (TLR4), CD14 and myeloid differentiation factor 88 (MyD88) as well as nuclear factor-κB were also suppressed by AAPC in ethanol-intoxicated rats. In conclusion, the protective effect of AAPC on ethanol-induced hepatotoxicity was mainly due to its ability to attenuate oxidative stress and inhibit Kupffer cell activation by decreasing the level of plasma endotoxin and the expression of TLR4, CD14 and MyD88.

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Section: Discussionmentioning

confidence: 99%

Retraction: Asiatic Acid from Potentilla chinensis Attenuate Ethanol-Induced Hepatic Injury via Suppression of Oxidative Stress and Kupffer Cell Activation

Wei

Huang

et al. 2013

Biological & Pharmaceutical Bulletin

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“…Chronic alcohol ingestion is known to be associated with defective gut motility that indirectly results in an elevated level of endotoxin in the liver 28) . Furthermore, the major metabolic product of alcohol, acetaldehyde activates hepatic stellate cells(HSCs), triggering inflammatory and fibrogenic signals, such as tumor necrosis factor(TNF), interleukins-6(IL-6) and transforming growth factor-1(TGF-1) 29) .…”

Section: ⅳ Discussionmentioning

confidence: 99%

Effect of Pharmacopuncture on Chronic Liver Injury in Rats

et al. 2015

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[Abstract]Objectives : Alcohol-related liver disease is a major cause of morbidity and mortality worldwide.The present study was undertaken to determine whether Ganoderma lucidum pharmacopuncture(GLP) could protect against chronic liver injury induced by ethanol intoxication in rats. Methods : Sprague-Dawley rats were divided into 4 groups: normal, control, normal saline pharmacopuncture(NP), and GLP, with 8 animals in each. Each group, except normal, received ethanol orally. The NP and GLP groups were treated daily with NP and GLP respectively. The control group was not treated. All rats except the normal group were intoxicated for 4 weeks by oral administration of EtOH(6 g/kg BW). Two acupuncture points were used: Qimen(LR 14 ) and Taechung(LR 3 ). Body weight, histopathological analysis, liver function, activities of antioxidant enzymes, and immunohistochemistry were assessed. Results : GLP reduced the histological changes due to chronic liver injury induced by EtOH and significantly reduced the increase in the alanine aminotransferase(ALT) and aspartate aminotransferase(AST) enzymes. It significantly reversed the superoxide dismutase(SOD) and the catalase activities(CAT). It also significantly decreased BAX and increased Bcl-2 immunoreactivity expression. Conclusions : This study showed the protective efficacy of GLP against EtOH-induced chronic liver injury in SD rats by modulating ethanol metabolizing enzymes activity, attenuating oxidative stress, and inhibiting mitochondrial damage-mediated apoptosis.

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“…87 Mechanisms that balance the barrier function of the gut and the ability of the liver to detoxify have been studied. 86,88 It was found that gut derived LPS played a significant role in several liver diseases. 89,90 Lu et al observed an increase in inflammatory responses as there was attrition of the protective ability of the liver to detoxify LPS derived from the gut.…”

Section: Connecting Gut and Livermentioning

confidence: 99%