Tao Zhi, Zhang Lihu, Wu Tao, Fang Xianying, Zhao Linguo
Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University, 159 Long Pan Road, Nanjing, 210037, China; College of Chemical Engineering, Nanjing Forestry University, 159 Long Pan Road, Nanjing, 210037, China.
Department of Pharmacy, Jiangsu Vocational College of Medicine, Yancheng, 224005, Jiangsu, China.
Food Chem Toxicol. 2021 Feb;148:111956. doi: 10.1016/j.fct.2020.111956. Epub 2020 Dec 27.
Alcoholic liver disease (ALD) is one of the most common health problems for drinkers, especially in men. Echinacoside (ECH), a natural phenylethanoid glycoside welcomed by the market, has been shown to have a variety of biological activities, such as neuroprotective, anti-fatigue, anti-diabetes and so on. Here, the protective effect and the underlying mechanism of ECH on ethanol-induced liver injuries were studied. In vitro, the HepG2 cells were treated with ECH prior to ethanol. In vivo, C57BL/6 J mice were fed a Lieber-DeCarli ethanol liquid diet and gave with or without 100 mg/kg ECH for 10 days. Our experiments showed that ECH significantly enhanced the levels of antioxidants and reduced the level of ROS, thus attenuating ethanol-induced oxidative stress. Besides, ECH attenuated lipid accumulation caused by ethanol, as evidenced by oil-red O staining, histological examination and the quantification of TG and TC. Finally, ECH increased the level of PPAR-α, and reduced the levels of SREBP-1c and FASN. When PPAR-α inhibitor was introduced in the system, the effects of ECH on SREBP-1c and FASN were reversed. Taken together, our study suggest that ECH can protect against ethanol-induced liver injuries via alleviating oxidative stress and hepatic steatosis by affecting SREBP-1c/FASN pathway via PPAR-α.
酒精性肝病(ALD)是饮酒者,尤其是男性中最常见的健康问题之一。紫锥菊苷(ECH)是一种受市场欢迎的天然苯乙醇苷,已被证明具有多种生物活性,如神经保护、抗疲劳、抗糖尿病等。在此,研究了ECH对乙醇诱导的肝损伤的保护作用及其潜在机制。在体外,乙醇处理前用ECH处理HepG2细胞。在体内,给C57BL/6 J小鼠喂食Lieber-DeCarli乙醇液体饲料,并给予或不给予100 mg/kg ECH,持续10天。我们的实验表明,ECH显著提高了抗氧化剂水平,降低了ROS水平,从而减轻了乙醇诱导的氧化应激。此外,油红O染色、组织学检查以及TG和TC定量结果表明,ECH减轻了乙醇引起的脂质积累。最后,ECH提高了PPAR-α水平,降低了SREBP-1c和FASN水平。当在系统中引入PPAR-α抑制剂时,ECH对SREBP-1c和FASN的作用被逆转。综上所述,我们的研究表明,ECH可通过PPAR-α影响SREBP-1c/FASN途径,减轻氧化应激和肝脂肪变性,从而预防乙醇诱导的肝损伤。