Abstract：
Objective: Hydroxytyrosol (HT) is a polyphenol with a wide range of biological activities. Excessive drinking can lead to oxidative stress and inflammation in the liver, which usually develop into alcohol liver disease (ALD). At present, there is no specific drug to treat ALD. In this paper, the protection effect of HT on ALD and the underline mechanism were studied.Methods: HepG2 cells were exposed to ethanol in vitro and C57BL/6J mice were fed with a Lieber-DeCarli ethanol liquid diet in vivo.Results: triglyceride (TG) level in serum and the expression of fatty acid synthase (FASN) were reduced significantly by the treatment with HT The acetaldehyde dehydrogenase (ALDH) activity was increased, the serum level of malondialdehyde (MDA) was decreased, catalase (CAT) and glutathione (GSH) were increased, suggesting that HT may reduce its oxidative damage to the body by promoting alcohol metabolism. Furthermore, according to the mRNA levels of tnf-α, il-6 and il-1β, HT inhibited ethanol-induced inflammation significantly. The anti-inflammatory mechanism of HT may be related to suppress the STAT3/iNOS pathway.Dissussion: Our study showed that HT could ameliorate ethanol-induced hepatic steatosis, oxidative stress and inflammation and provide a new candidate for the prevention and treatment of ALD.
摘要：
目的:羟基酪醇(HT)是一种具有广泛生物活性的多酚。过度饮酒会导致肝脏氧化应激和炎症，通常发展为酒精性肝病（ALD）。目前,没有特定的药物来治疗ALD。在本文中,研究了HT对ALD的保护作用及其机理。方法：将HepG2细胞体外暴露于乙醇中，并在体内饲喂C57BL/6J小鼠Lieber-DeCarli乙醇液体饮食。结果:血清甘油三酯(TG)水平和脂肪酸合成酶(FASN)表达显著降低,乙醛脱氢酶(ALDH)活性升高,血清丙二醛（MDA）水平降低，过氧化氢酶（CAT）和谷胱甘肽（GSH）增加，提示HT可能通过促进酒精代谢减少其对机体的氧化损伤。此外，根据tnf-α的mRNA水平，il-6和il-1β，HT显著抑制乙醇诱导的炎症。HT的抗炎机制可能与抑制STAT3/iNOS通路有关。破裂：我们的研究表明HT可以改善乙醇诱导的肝脏脂肪变性，氧化应激和炎症反应,为ALD的预防和治疗提供新的候选者。
