Aloin protects against chronic alcoholic liver injury via attenuating lipid accumulation, oxidative stress and inflammation in mice

2014 ◽  
Vol 37 (12) ◽  
pp. 1624-1633 ◽  
Author(s):  
Yan Cui ◽  
Qing Ye ◽  
Heya Wang ◽  
Yingchao Li ◽  
Xiuhua Xia ◽  
...  
Life Sciences ◽  
2019 ◽  
Vol 216 ◽  
pp. 305-312 ◽  
Author(s):  
Chuying Zhou ◽  
Yuling Lai ◽  
Peng Huang ◽  
Lingpeng Xie ◽  
Haiyan Lin ◽  
...  

2000 ◽  
Vol 118 (4) ◽  
pp. A924
Author(s):  
Xiuhui Zhong ◽  
Zhanxiang Zhou ◽  
Y. James Kang

2017 ◽  
Vol 267 ◽  
pp. 1-10 ◽  
Author(s):  
Ning Zhang ◽  
Yan Hu ◽  
Chunchun Ding ◽  
Wenjing Zeng ◽  
Wen Shan ◽  
...  

Gut ◽  
2016 ◽  
Vol 66 (4) ◽  
pp. 705-715 ◽  
Author(s):  
Man Li ◽  
Yong He ◽  
Zhou Zhou ◽  
Teresa Ramirez ◽  
Yueqiu Gao ◽  
...  

2009 ◽  
Vol 62 (11-12) ◽  
pp. 547-553 ◽  
Author(s):  
Tatjana Radosavljevic ◽  
Dusan Mladenovic ◽  
Danijela Vucevic

Introduction. Oxidative stress plays an important role in pathogenesis of alcoholic liver injury. The main source of free oxygen species is cytochrome P450-dependent monooxygenase, which can be induced by ethanol. Role of cytochrome P4502E1 in ethanol-induced oxidative stress. Reactive oxygen species produced by this enzyme are more important in intracellular oxidative damage compared to species derived from activated phagocytes. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in alcohol-induced oxidative stress. Production of mitochondrial reactive oxygen species is increased, and glutathione content is decreased in chronically ethanolfed animals. Oxidative stress in mitochondria leads to mitochondrial DNA damage and has a dual effect on apoptosis. Role of Kupffer cells in alcohol-induced liver injury. Chronic ethanol consumption is associated with increased release of endotoxin from gut lumen into portal circulation. Endotoxin activates Kupffer cells, which then release proinflammatory cytokines and oxidants. Role of neutrophils in alcohol-induced liver injury. Alcoholic liver injury leads to the accumulation of neutrophils, which release reactive oxygen species and lysosomal enzymes and contribute to hepatocyte damage and necrosis. Role of nitric oxide in alcohol-induced oxidative stress. High amounts of nitric oxide contribute to the oxidative damage, mainly by generating peroxynitrites. Role of antioxidants in ethanol-induced oxidative stress. Chronic ethanol consumption is associated with reduced liver glutathione and ?-tocopherol level and with reduced superoxide dismutase, catalase and glutathione peroxidase activity. Conclusion. Oxidative stress in alcoholic liver disease is a consequence of increased production of oxidants and decreased antioxidant defense in the liver.


2016 ◽  
Vol 186 (12) ◽  
pp. 3117-3130 ◽  
Author(s):  
Yanqing Zhang ◽  
Cheng Wang ◽  
Yunli Tian ◽  
Fengxiao Zhang ◽  
Wenjing Xu ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Jing-Hua Peng ◽  
Tuan Cui ◽  
Zhao-Lin Sun ◽  
Fu Huang ◽  
Liang Chen ◽  
...  

Kudzu (Pueraria lobata) is one of the earliest medicinal plants used to treat alcohol abuse in traditional Chinese medicine for more than a millennium. However, little is known about its effects on chronic alcoholic liver injury. Therefore, the present study observed the effects of puerariae radix extract (RPE) on chronic alcoholic liver injury as well as Kupffer cells (KCs) activation to release tumor necrosis factor alpha (TNF-α) induced by gut-derived endotoxin in rats and macrophage cell line. RPE was observed to alleviate the pathological changes and lipids deposition in liver tissues as well as the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and hepatic gamma-glutamyl transpeptidase (GGT) activity. Meanwhile, RPE inhibited KCs activation and subsequent hepatic TNF-αexpression and downregulated the protein expression of endotoxin receptors, lipopolysaccharide binding protein (LBP), CD14, Toll-like receptor (TLR) 2, and TLR4 in chronic alcohol intake rats. Furthermore, anin vitrostudy showed that RPE inhibited the expression of TNF-αand endotoxin receptors, CD14 and TLR4, induced by LPS in RAW264.7 cells. In summary, this study demonstrated that RPE mitigated liver damage and lipid deposition induced by chronic alcohol intake in rats, as well as TNF-αrelease, protein expression of endotoxin receptorsin vivoorin vitro.


RSC Advances ◽  
2018 ◽  
Vol 8 (43) ◽  
pp. 24399-24410 ◽  
Author(s):  
Qiong-Hui Huang ◽  
Xue Wu ◽  
Xiao-Hong Chen ◽  
Jia-Zhen Wu ◽  
Zi-Ren Su ◽  
...  

Excessive alcohol consumption can cause serious hepatic injury which is associated with oxidative stress and fatty metabolic disturbance.


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