College of Pharmacy, Guilin Medical University, Guilin 541004, Guangxi, China.
College of Pharmacy, Gansu University of Chinese Medicine, Lanzhou 730000, Gansu, China.
Life Sci. 2020 Dec 1;262:118546. doi: 10.1016/j.lfs.2020.118546. Epub 2020 Oct 6.
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-κB and Nrf2/HO-1 pathways.
研究表明，蒲公英甾醇（TAR）在治疗免疫性肝损伤和酒精性肝损伤方面有效。其作用机制主要与抑制炎症有关。为了确定 TAR 缓解乙醇和高脂肪饮食诱导的肝损伤的关键分子机制，我们检查了病理形态、生化、氧化应激、炎症反应和脂质代谢。结果表明，TAR 可抑制乙醇诱导的肝细胞死亡或脂质积累，并抑制氧化应激、炎症反应和脂质代谢紊乱。更具体地说，TAR 可下调乙醇诱导的 TLR-4 和 MyD88 炎症反应。当用 TAR 处理时，对增加的氧化应激作出反应而产生的 CYP2E1、Nrf2 和 HO-1 的产生受到调节。总之，TAR 可抑制炎症反应和氧化应激，这与 TAR 对 TLR-4/MyD88/NF-κB 和 Nrf2/HO-1 途径的调节有关。
