Diallyl trisulfide attenuates carbon tetrachloride-caused liver injury and fibrogenesis and reduces hepatic oxidative stress in rats

2014 ◽  
Vol 387 (5) ◽  
pp. 445-455 ◽  
Author(s):  
Xiaojing Zhu ◽  
Feng Zhang ◽  
Liang Zhou ◽  
Desong Kong ◽  
Li Chen ◽  
...  
2020 ◽  
Vol 11 (5) ◽  
pp. 4485-4498
Author(s):  
Fuchuan Guo ◽  
Xinyun Zhuang ◽  
Mengyuan Han ◽  
Wenting Lin

EPP protected against hepatic injury induced by CCl4-derived reactive intermediates through the suppression of hepatic oxidative stress, inflammation, and apoptosis.


2021 ◽  
Vol 97 ◽  
pp. 107716
Author(s):  
Ya-Qi Wang ◽  
Xiao-Pan Geng ◽  
Ming-Wei Wang ◽  
Hong-Qian Wang ◽  
Cheng Zhang ◽  
...  

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Chun-Qiu Hu ◽  
Qing-Li Bo ◽  
Lan-Lan Chu ◽  
Yong-Di Hu ◽  
Lin Fu ◽  
...  

Vitamin D deficiency has been reported in alcoholics. This study is aimed at evaluating the effects of vitamin D deficiency on chronic alcohol-induced liver injury in mice. Mice were fed with modified Lieber-DeCarli liquid diets for 6 weeks to establish an animal model of chronic alcohol-induced liver injury. In the VDD+EtOH group, mice were fed with modified diets, in which vitamin D was depleted. Vitamin D deficiency aggravated alcohol-induced liver injury. Furthermore, vitamin D deficiency aggravated hepatocyte apoptosis during alcohol-induced liver injury. Although it has a little effect on hepatic TG content, vitamin D deficiency promoted alcohol-induced hepatic GSH depletion and lipid peroxidation. Further analysis showed that vitamin D deficiency further increased alcohol-induced upregulation of hepatic inducible nitric oxide synthase (inos), two NADPH oxidase subunits p47phox and gp91phox, and heme oxygenase- (HO-) 1. By contrast, vitamin D deficiency attenuated alcohol-induced upregulation of hepatic antioxidant enzyme genes, such as superoxide dismutase (sod) 1 and gshpx. In addition, vitamin D deficiency significantly elevated alcohol-induced upregulation of hepatic proinflammatory cytokines and chemokines. Taken together, these results suggest that vitamin D deficiency aggravates hepatic oxidative stress and inflammation during chronic alcohol-induced liver injury.


2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Qingshan Chen ◽  
Qi Zhan ◽  
Ying Li ◽  
Sen Sun ◽  
Liang Zhao ◽  
...  

Schisandra chinensis(S. chinensis) is a traditional Chinese herbal medicine widely used for the treatment of liver disease, whose main active components are lignans. However, the action mechanisms of the lignans inS. chinensisremain unclear. This study aimed to investigate the protective effect and related molecular mechanism ofSchisandralignan extract (SLE) against carbon tetrachloride- (CCl4-) induced acute liver injury in mice. Different doses of SLE at 50, 100, and 200 mg/kg were administered daily by gavage for 5 days before CCl4treatment. The results showed that SLE significantly decreased the activities of serum ALT/AST and reduced liver pathologic changes induced by CCl4. Pretreatment with SLE not only decreased the content of MDA but increased SOD, GSH, and GSH-Px activities in the liver, suggesting that SLE attenuated CCl4-induced oxidative stress. The expression levels of inflammatory cytokines TNF-a, IL-1β, and IL-6 were decreased after oral administration of SLE, probably because lignans inhibited the NF-κB activity. Additionally, SLE also inhibited hepatocyte apoptosis by suppressing JNK activation and regulating Bcl-2/Bax signaling pathways. In conclusion, these results suggested that SLE prevented CCl4-induced liver injury through a combination of antioxidative stress, anti-inflammation, and antihepatocyte apoptosis and alleviated inflammation and apoptosis by regulating the NF-κB, JNK, and Bcl-2/Bax signaling pathways.


2007 ◽  
Vol 100 (2) ◽  
pp. 115-120 ◽  
Author(s):  
Zhi-ming Wu ◽  
Tao Wen ◽  
Yu-fen Tan ◽  
Yan Liu ◽  
Feng Ren ◽  
...  

BioFactors ◽  
2004 ◽  
Vol 21 (1-4) ◽  
pp. 171-174 ◽  
Author(s):  
Tomomi Fukao ◽  
Takashi Hosono ◽  
Satomi Misawa ◽  
Taiichiro Seki ◽  
Toyohiko Ariga

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