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Effects of taraxasterol against ethanol and high-fat diet-induced liver injury by regulating TLR4/MyD88/NF-κB and Nrf2/HO-1 signaling pathways  ( SCI-EXPANDED收录)   被引量:25

文献类型:期刊文献

英文题名:Effects of taraxasterol against ethanol and high-fat diet-induced liver injury by regulating TLR4/MyD88/NF-κB and Nrf2/HO-1 signaling pathways

作者:Li, Zimeng[1];Lian, Yuanyu[1];Wei, Riming[1];Jin, Ling[2];Cao, Houkang[2];Zhao, Tanglian[1];Ma, Xiaohui[2];Zhong, Mingli[1];Gao, Ya[1,2];Zhang, Kefeng[1]

第一作者:Li, Zimeng

通信作者:Gao, Y[1];Zhang, KF[1];Gao, Y[2]

机构:[1]Guilin Med Univ, Coll Pharm, Guilin 541004, Guangxi, Peoples R China;[2]Gansu Univ Chinese Med, Coll Pharm, Lanzhou 730000, Gansu, Peoples R China

第一机构:Guilin Med Univ, Coll Pharm, Guilin 541004, Guangxi, Peoples R China

通信机构:[1]corresponding author), Guilin Med Univ, Coll Pharm, Guilin 541004, Guangxi, Peoples R China;[2]corresponding author), Gansu Univ Chinese Med, Coll Pharm, Lanzhou 730000, Gansu, Peoples R China.|[1073501e14fb35863569f]甘肃中医药大学药学院(西北中藏药协同创新中心办公室);[10735]甘肃中医药大学;

年份:2020

卷号:262

外文期刊名:LIFE SCIENCES

收录:;Scopus(收录号:2-s2.0-85092147457);WOS:【SCI-EXPANDED(收录号:WOS:000593979900003)】;

基金:Contract grant sponsor: National Natural Science Foundation of CHN. Contract grant numbers: National Natural Science Foundation of CHN (81960779, 81760114, 81660104, and 81860673); Natural Science Foundation of Guangxi Province of CHN (2017GXNSFAA198218, 2017GXNSFAA198326 and 2018GXNSFAA281040).

语种:英文

外文关键词:Taraxasterol; Ethanol; High-fat diet; TLR4/MyD88/NF-kappa B; Nrf2/HO-1

摘要:Studies have reported that taraxasterol (TAR) is effective in the treatment of immune liver injury and alcoholic liver injury. The mechanism of action is mainly related to the inhibition of inflammation. To determine the key molecular mechanisms for the effect of TAR on alleviating ethanol and high-fat diet-induced liver injury, pathological morphology, biochemistry, oxidative stress, inflammatory response and lipid metabolism were examined. Our results showed that TAR could inhibit ethanol-induced hepatocyte death or lipid accumulation, and suppress oxidative stress, inflammatory response and lipid metabolism disorders. More specifically, ethanol induced TLR-4 and MyD88 inflammatory response were down-regulated, when treated with TAR. Production of CYP2E1, Nrf2 and HO-1, which produced in response to increased oxidative stress, were regulated in TAR treated, ethanol-induced hepatocytes. In summary, TAR could inhibit the inflammatory response and oxidative stress, which was related to the regulation of TAR on TLR-4/MyD88/NF-kappa B and Nrf2/HO-1 pathways.

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