Hepatoprotective Effect of Allium ochotense Extracts on Chronic Alcohol-Induced Fatty Liver and Hepatic Inflammation in C57BL/6 Mice

被引:2
作者
Go, Min Ji [1 ]
Kim, Jong Min [1 ]
Lee, Hyo Lim [1 ]
Kim, Tae Yoon [1 ]
Kim, Ju Hui [1 ]
Lee, Han Su [1 ]
Kim, In Young [1 ]
Sim, Seon Jeong [2 ]
Heo, Ho Jin [1 ]
机构
[1] Gyeongsang Natl Univ, Inst Agr & Life Sci, Div Appl Life Sci BK21, Jinju 52828, South Korea
[2] Gyeongsangnam Do Forest Environm Res Inst, Forest Res Dept, Jinju 52615, South Korea
关键词
Allium ochotense; alcoholic liver disease; lipid metabolism; alcoholic hepatitis; apoptosis; liver fibrosis; FERULIC ACID; MITOCHONDRIA; PATHOGENESIS; MECHANISMS; ETHANOL;
D O I
10.3390/ijms25063496
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
This study was performed to investigate the protective effects of Allium ochotense on fatty liver and hepatitis in chronic alcohol-induced hepatotoxicity. The physiological compounds of a mixture of aqueous and 60% ethanol (2:8, w/w) extracts of A. ochotense (EA) were identified as kestose, raffinose, kaempferol and quercetin glucoside, and kaempferol di-glucoside by UPLC Q-TOF MSE. The EA regulated the levels of lipid metabolism-related biomarkers such as total cholesterol, triglyceride, low-density lipoprotein (LDL), and high-density lipoprotein (HDL)-cholesterol in serum. Also, EA ameliorated the levels of liver toxicity-related biomarkers such as glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and total bilirubin in serum. EA improved the antioxidant system by reducing malondialdehyde contents and increasing superoxide dismutase (SOD) levels and reduced glutathione content. EA improved the alcohol metabolizing enzymes such as alcohol dehydrogenase, acetaldehyde dehydrogenase, and cytochrome P450 2E1 (CYP2E1). Treatment with EA alleviated lipid accumulation-related protein expression by improving phosphorylation of AMP-activated protein kinase (p-AMPK) expression levels. Especially, EA reduced inflammatory response by regulating the toll-like receptor-4/nuclear factor kappa-light-chain-enhancer of activated B cells (TLR-4/NF-kappa B) signaling pathway. EA showed an anti-apoptotic effect by regulating the expression levels of B-cell lymphoma 2 (BCl-2), BCl-2-associated X protein (BAX), and caspase 3. Treatment with EA also ameliorated liver fibrosis via inhibition of transforming growth factor-beta 1/suppressor of mothers against decapentaplegic (TGF-beta 1/Smad) pathway and alpha-smooth muscle actin (alpha-SMA). Therefore, these results suggest that EA might be a potential prophylactic agent for the treatment of alcoholic liver disease.
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页数:25
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