Effects of taraxasterol against ethanol and high-fat diet-induced liver injury by regulating TLR4/MyD88/NF-κB and Nrf2/HO-1 signaling pathways
Effects of taraxasterol against ethanol and high-fat diet-induced liver injury by regulating TLR4/MyD88/NF-κB and Nrf2/HO-1 signaling pathways
复制标题
蒲公英甾醇通过调节TLR4/MyD88/NF-kappa B和Nrf2/HO-1信号通路对抗乙醇和高脂饮食引起的肝损伤
DOI：
10.1016/j.lfs.2020.118546
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发表时间：
2020-12-01
期刊：
影响因子：
6.1
通讯作者：
Zhang, Kefeng
中科院分区：
文献类型：
--
作者：
Li, Zimeng;Lian, Yuanyu;Zhang, Kefeng
有研究报道，taraxasterol （TAR）可有效治疗免疫性肝损伤和酒精性肝损伤。其作用机制主要与抑制炎症有关。通过病理形态学、生物化学、氧化应激、炎症反应和脂质代谢等方面的研究，探讨TAR减轻乙醇和高脂饮食引起的肝损伤的关键分子机制。我们的研究结果表明，TAR可以抑制乙醇诱导的肝细胞死亡或脂质积累，抑制氧化应激、炎症反应和脂质代谢紊乱。更具体地说，当用TAR治疗时，乙醇诱导的TLR-4和MyD88炎症反应下调。在TAR处理的乙醇诱导的肝细胞中，因氧化应激增加而产生的CYP2E1、Nrf2和HO-1的产生受到调节。综上所述，TAR能够抑制炎症反应和氧化应激，这与TAR对TLR-4/MyD88/NF-kappa B和Nrf2/HO-1通路的调控有关。
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.