PMC:4277126 / 68008-71346 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/4277126","sourcedb":"PMC","sourceid":"4277126","source_url":"http://www.ncbi.nlm.nih.gov/pmc/4277126","text":"Alcoholic liver disease or alcoholic fatty liver disease\nAlcohol use was the third leading risk factor contributing to the global burden of disease after high blood pressure and tobacco smoking. According to a WHO 2008 report, alcohol causes 1.8 million annual deaths globally and accounts for 4.0% of the total disease burden.86 Alcoholic liver disease or alcoholic fatty liver disease (AFLD) is a chronic multistep disease with fatty accumulation in the liver due to chronic alcohol overconsumption, which typically progresses through the stages of fatty liver or simple steatosis, alcoholic hepatitis, and chronic hepatitis with hepatic fibrosis or cirrhosis.87,88 Chronic consumption of alcohol results in the secretion of proinflammatory cytokines such as TNF-α, IL-6 and IL-8, oxidative stress, lipid peroxidation, and acetaldehyde toxicity.87,88 These factors cause inflammation, apoptosis, and eventually, fibrosis and cirrhosis of the liver. As one of the most prevalent liver diseases caused by alcohol overconsumption, AFLD affects over 2 million people in the US. In the People’s Republic of China, it is estimated that 2.8% of population has AFLD or suspected AFLD. There is no cure for alcoholic liver disease,89 and natural compounds with potent antioxidative effects have been used to treat alcoholic liver disease.\nCheng and Kong90 investigated the protective effect of LBPs on alcohol-induced liver injury in rats. Rats were fed with 7 g ethanol/kg body weight by gastric infusion three times a day, for 30 consecutive days, to make the liver injury model. Ethanol treatment significantly increased serum alanine aminotransferase and AST, triglycerides, total cholesterol, low-density lipoprotein cholesterol (LDL-C), and MDA levels but decreased serum high-density lipoprotein cholesterol (HDL-C) and hepatic SOD, CAT, GPx, and GSH.90 Administration of 300 mg/kg LBPs for 30 days significantly reversed these ethanol-induced effects, reduced liver injury, prevented the progression of alcohol-induced fatty liver, and improved the antioxidant function when compared with the ethanol group. The results indicate that LBPs protect the liver from ethanol-induced injuries via antioxidation.\nXiao et al91 investigated whether thioredoxin-interacting protein (TXNIP) and NOD-like receptor 3 (NLRP3) inflammasome mediated the attenuation of ethanol-induced hepatic injury by LBPs using the rat normal hepatocyte line BRL-3A cells. Cells were pretreated with LBPs prior to ethanol incubation. Hepatic damages including apoptosis, inflammation, and oxidative stress were monitored. TXNIP was knocked down using specific small interfering RNA. The study showed that 50 µg/mL LBP pretreatment significantly alleviated 24-hour ethanol-induced overexpression of TXNIP, increased cellular apoptosis, secretion of inflammatory cytokines, activation of NLRP3 inflammasome, production of ROS, and reduced antioxidant enzyme expression.91 Silence of TXNIP suppressed the activated NLRP3 inflammasome, increased oxidative stress, and worsened apoptosis in the cells. Further addition of LBPs did not affect the effects of TXNIP inhibition on BRL-3A cells.91 These results indicate that inhibition of hepatic TXNIP by LBPs contributes to the reduction of cellular apoptosis, oxidative stress, and NLRP3 inflammasome-mediated 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