PMC:4277126 / 67982-77431 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":"Hepatoprotective effects\n\nAlcoholic 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 inflammation.\n\nNonalcoholic fatty liver disease\nNonalcoholic fatty liver disease (NAFLD) is a chronic metabolic liver disease that histologically resembles the alcohol-induced hepatic injury, but is not caused by alcohol abuse.92,93 It is a spectrum of disease ranging from simple steatosis, to non-alcoholic steatohepatitis, through to advanced fibrosis and cirrhosis. NAFLD is associated with other medical conditions such as metabolic syndrome, obesity, cardiovascular disease, and diabetes.92,93 Mechanisms involved in the pathogenesis are associated with diet and lifestyle, influx of free fatty acids to the liver from adipose tissue due to insulin resistance, hepatic oxidative stress, cytokines production, reduced very low-density lipoprotein secretion, and intestinal microbiome.94 In Western countries, NAFLD affects 20%–40% of the adult populations. Weight loss through improved diet and increased physical activity has been the cornerstone therapy of NAFLD, but no drugs are approved for use in NAFLD.93,95\nIn a study conducted by Xiao et al96,97 female rats were fed with a high-fat diet (HD) to induce nonalcoholic steatohepatitis, with or without an oral 1 mg/kg LBP feeding, daily for 8 weeks. LBP-treated rats showed improved histology and free fatty acid levels, rebalance of lipid metabolism, reduction in profibrogenic factors through the transforming growth factor (TGF)-β/small mothers against decapentaplegic pathway, improved oxidative stress through cytochrome P450 2E1-dependent pathway, reduction in hepatic proinflammatory mediators and chemokine production, and amelioration of hepatic apoptosis through the p53-dependent intrinsic and extrinsic pathways.96\nA mouse study by Li et al98 investigated whether LBPs prevented fatty liver through activation of adenosine monophosphate-activated protein kinase (AMPK) and suppression of sterol regulatory element-binding protein-1c (SREBP-1c).98 Male C57BL/6J mice were fed a low-fat diet, HD, or 100 mg/kg LBP-treatment diet for 24 weeks. The results showed that LBPs improved body compositions and lipid metabolic profiles in high-fat diet-fed mice. Oil Red O staining showed that LBPs significantly reduced hepatic intracellular triacylglycerol accumulation. Hepatic genes expression profiles demonstrated that LBPs activated the phosphorylation of AMPK, suppressed nuclear expression of SREBP-1c, and decreased protein and mRNA expression of lipogenic genes.98\nLin et al99 investigated whether AMPKα2 is essential for the protective effects of wolfberries on mitochondrial dysfunction and subsequent hepatic steatosis in mice. Six-week-old male AMPKα2 knockout mice and genetic background C57BL/6J mice were fed a control, HD (45% [kilocalorie] fat), and/or HD with 5% (kilocalorie) wolfberry diets for 18 weeks. HD feeding for 18 weeks lowered hepatic lutein and zeaxanthin contents, inhibited protein expression of β,β-carotene 9′,10′-oxygenase 2 and heat shock protein 60 (HSP60) in mitochondria, increased reactive oxygen species level, suppressed mitophagy and mitochondrial biogenesis as determined by accumulation of p62, inhibited phosphorylation of Unc-51-like kinase 1 on Ser555, and decreased expression of peroxisome proliferator-activated receptor-γ coactivator 1α, resulting in hepatic steatosis in AMPKα2 knockout and C57BL/6J mice.99 Dietary wolfberry elevated the xanthophyll concentrations and enhanced expression of β,β-carotene 9′,10′-oxygenase 2 and HSP60, attenuated mitochondrial oxidative stress, activated AMPKα2, potentiated mitophagy and mitochondrial biogenesis, and enhanced lipid oxidation and secretion in the liver of C57BL/6J mice.99 Dietary wolfberry selectively activated AMPKα2, enhanced mitochondrial biogenesis, and potentiated mitophagy, leading to the prevention of hepatic steatosis in obese mice.\n\nCarbon tetrachloride-induced acute liver injury\nA mouse study100 on the protective effect of LBPs was conducted in carbon tetrachloride (CCl4)-induced acute liver injury. Mice were intraperitoneally injected with CCl4 to induce acute hepatotoxicity and were orally fed with LBPs 2 hours before the CCl4 injection. The results showed that LBPs reduced necroinflammation and oxidative stress induced by CCl4. The protective effects of LBPs against CCl4-induced hepatotoxicity were partly through the downregulation of NF-κB activity.100 NF-κB plays a key role in regulating the immune response to stimuli such as stress, cytokines, free radicals, ultraviolet irradiation, and infection.101 While in an inactivated state, NF-κB is located in the cytosol complexed with the inhibitory protein IκBα. The activated NF-κB will be translocated into the nucleus where it binds to specific sequences of DNA called response elements. The DNA/NF-κB complex then recruits other proteins such as coactivators and RNA polymerase to trigger gene expression.101\nAhn et al102 investigated whether Lycium chinense (LC) fruit extract and its component betaine could affect CCl4-induced hepatotoxicity in rats. The treatment of L. chinense fruit extract significantly suppressed the increase of serum alanine aminotransferase and AST in CCl4-injured rats; restored the decreased levels of anti-oxidant enzymes, such as total antioxidant capacity, SOD, CAT, and GPx; and suppressed the expression of inflammatory mediators including inducible nitric oxide synthase and cyclooxygenases.102 Betaine showed hepatoprotective effects as that of L. chinense fruit extract. These findings imply that LC fruit extract reduced CCl4-induced hepatic injury via increasing antioxidative activity and decreasing inflammatory mediators including inducible nitric oxide synthase and cyclooxygenases.\n\nSummary on the hepatoprotective effects of LBPs\nTaken together, LBPs can substantially reduce oxidative stress, suppress inflammatory responses, and inhibit apoptosis to protect liver from injuries due to various insults. LBPs increase the levels and activities of GPx, SOD, CAT, GSH, HDL-C, and AMPK, but reduce the levels of LDL-C and MDA via modulation of p53-, SREBP-1c-, and NF-κB-mediated pathways (Figure 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