Abstract
Natural polysaccharides, particularly galactomannans, are potential candidates for treatment of alcoholic liver diseases (ALD). However, applications are restricted due to the physicochemical properties associated with the high molecular weight. In this work, guar gum galactomannans were partially hydrolyzed by β-mannanase, and the molecular mechanisms of hepatoprotective effects were elucidated both in vitro and in vivo. Release of lactate dehydrogenase and cytochrome C were attenuated by partially hydrolyzed guar gum (PHGG) in HepG2 cells, due to protected cell and mitochondrial membrane integrity. PHGG co-administration decreased serum amino transaminases and cholinesterase levels of acute alcohol intoxicated mice, while hepatic pathologic morphology was depleted. Activity of superoxide dismutase, catalase, and glutathione peroxidase was recovered to 198.2, 34.5, 236.0 U/mg protein, respectively, while malondialdehyde level was decreased by 76.3% (PHGG, 1000 mg/kg∙day). Co-administration of PHGG induced a 4.4-fold increment of p-AMPK expression, and lipid metabolism was mediated. PHGG alleviated toll-like-receptor-4-mediated inflammation via the signaling cascade of MyD88 and IκBα, decreasing cytokine production. Moreover, mediated expression of Bcl-2 and Bax was responsible for inhibited acute alcohol-induced apoptosis with suppressed cleavage of caspase 3 and PARP. Findings gained suggest that PHGG can be used as functional food supplement for the treatment of acute alcohol-induced liver injury.
Highlights
IntroductionMisuse of alcohol has been considered one of the most common cause of liver diseases
Alcoholic liver diseases (ALD), ranging from liver fibrosis to end-stage cirrhosis, account for approximately 1–4% of the total burden of diseases worldwide (World Health Organization, WHO) [1,2].Misuse of alcohol has been considered one of the most common cause of liver diseases
Various pathways have been identified to be responsible for the pathological process of ALD, such as oxidative stress, inflammation, and apoptosis [1,4]
Summary
Misuse of alcohol has been considered one of the most common cause of liver diseases. Life threatening complications of portal hypertension, liver failure, and increased incidence of hepatocellular carcinoma are related to the prevalent usage of alcohol [3]. ALD is characterized by a complex spectrum of histological lesions, such as steatosis and cirrhosis. Those basic lesions can occur separately, simultaneously, or sequentially in the same patient [2]. Various pathways have been identified to be responsible for the pathological process of ALD, such as oxidative stress, inflammation, and apoptosis [1,4]
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