Abstract
Alcoholic liver disease (ALD) has become one of the major global health problems, with augmented morbidity and mortality. Evidence indicates that flavonoids can reduce the risk of ALD owing to their biological properties. However, the effect of structurally different flavonoid subclasses on alleviating alcohol-induced liver damage in a same model has never been studied. In this study, mice were supplemented with five kinds of flavonoid subgroups, apigenin (flavone), quercetin (flavonol), naringenin (flavanone), (-)-epigallocatechin gallate (flavanol), and genistein (isoflavone), in the same dose (0.3 mmol kg−1 body weight) and then given 50% alcohol by gastric perfusion for five consecutive weeks. The results demonstrated that genistein and naringenin had greater benefits in terms of mitigating fibrosis and apoptosis, respectively, in the liver. Lipid deposition, partial inflammatory-related factors (nuclear factor kappa B p65, cyclooxygenase-2, and interleukin-6 levels), and hepatic histopathological alterations were similarly attenuated by five kinds of flavonoids. All the flavonoids also showed different degrees of influence on protecting against alcoholic liver injury on other aspects, such as serum biochemistry makers, hepatic lipid accumulation, lipid peroxidation, antioxidant capacities, and inflammation.
Highlights
Per capita alcohol consumption has risen rapidly in many countries, and excessive alcohol consumption, the third largest risk for disease in the world, has increased morbidity and mortality from alcoholic liver disease (ALD), which has become one of the most critical public health issues [1,2,3].excessive alcohol consumption can aggravate economic burdens on society, and leadsNutrients 2018, 10, 1754; doi:10.3390/nu10111754 www.mdpi.com/journal/nutrients Nutrients FOR PEER REVIEW 10, x175422 of of 14 to about 3 million deaths annually [1,4]
We aimed to investigate the differences in the effects of purified flavone, flavonol, flavanone, flavanol (EGCG), and isoflavone on liver injury by alcohol in mice
P65, transforming growth factor β1 (TGF-β1), cyclooxygenase-2 (COX-2), monocyte chemoattractant protein-1 (MCP-1), inducible nitric oxide synthase, TNF-α, IL-6, and caspase-3 were obtained from Keyingmei Biotechnology and Science Inc. (Beijing, China)
Summary
Per capita alcohol consumption has risen rapidly in many countries, and excessive alcohol consumption, the third largest risk for disease in the world, has increased morbidity and mortality from alcoholic liver disease (ALD), which has become one of the most critical public health issues [1,2,3].excessive alcohol consumption can aggravate economic burdens on society, and leadsNutrients 2018, 10, 1754; doi:10.3390/nu10111754 www.mdpi.com/journal/nutrients Nutrients FOR PEER REVIEW 10, x175422 of of 14 to about 3 million deaths annually [1,4]. Usually elicits series of histological phenotypes alcohol-related liverdeaths injury,annually including the ALD earliest response of afatty liver or simple steatosis (an of alcohol-related liver injury, including the earliest response of fatty liver or simple steatosis accumulation of fat in hepatocytes), steatohepatitis (steatosis with superimposed inflammatory (an accumulation of fat in hepatocytes), steatohepatitis (steatosis with superimposed inflammatory infiltrate), and ultimate progression to fibrosis, cirrhosis, and hepatocellular carcinoma [5]. These infiltrate), and ultimate progression to fibrosis, carcinoma [5]. At present,cytokines, there is increasing seeking ideal dysfunction, etc. [6,7].asAtalternatives, present, there is increasing in seeking ideal and safe components and safe components especially from interest plant sources, for the amelioration of ALD in as alternatives, especially from with plantside sources, for[8]
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