Faculty of Food Science and Engineering, Kunming University of Science and Technology, Kunming, 650500, China.
National and Local Joint Engineering Research Center for Green Preparation Technology of Biobased Materials, Yunnan Minzu University, Kunming, 650500, China.
Food Funct. 2022 May 10;13(9):5299-5316. doi: 10.1039/d2fo00507g.
Que Zui tea (QT), a traditional herbal tea in China, has a significant hepatoprotective effect. 6'--Caffeoylarbutin (CA) is the most abundant chemical compound in the QT. However, the hepatoprotective effect of CA has not been investigated. This study is aimed to evaluate the protective effect of CA on acetaminophen (APAP) induced hepatotoxicity and and its possible underlying mechanism. In APAP-induced HepG-2 cells, CA inhibited intracellular ROS accumulation and cell apoptosis, and improved the expression of antioxidants including SOD, CAT and GSH. In APAP-administrated mice, CA pretreatment remarkably ameliorated the histopathological damage and inflammatory response, and antioxidant enzyme activity in the serum and liver tissues. Moreover, the immunohistochemistry and immunofluorescence assay results revealed that the CA markedly reduced ROS production and apoptosis, and activated antioxidant transcription factor Nrf2 in the liver. Meanwhile, molecular docking results showed that the strong binding force of CA and PI3K was due to the higher number of hydrogen- and π-bonds with active site residues. Notably, CA pretreatment significantly regulated the expression of PI3K, Akt, Nrf2, NQO1, HO-1, Bcl-2, Bax, caspase-3, and caspase-9 proteins in APAP-treated liver tissues. These data demonstrated that CA had a protective effect against APAP-induced hepatotoxicity regulating the PI3K/Akt and Nrf2 signaling pathway.
曲孜茶（QT）是中国的一种传统草药茶，具有显著的保肝作用。6'-咖啡酰基奎宁酸（CA）是 QT 中含量最丰富的化学化合物。然而，CA 的保肝作用尚未得到研究。本研究旨在评估 CA 对乙酰氨基酚（APAP）诱导的肝毒性的保护作用及其可能的机制。在 APAP 诱导的 HepG-2 细胞中，CA 抑制细胞内 ROS 积累和细胞凋亡，并改善抗氧化剂 SOD、CAT 和 GSH 的表达。在给予 APAP 的小鼠中，CA 预处理可显著改善肝组织的组织病理学损伤和炎症反应，以及血清和肝组织中抗氧化酶的活性。此外，免疫组织化学和免疫荧光分析结果表明，CA 可显著减少 ROS 产生和细胞凋亡，并激活肝脏中的抗氧化转录因子 Nrf2。同时，分子对接结果表明，CA 与 PI3K 的强结合力是由于与活性位点残基形成的氢键和π键数量较多。值得注意的是，CA 预处理可显著调节 APAP 处理的肝组织中 PI3K、Akt、Nrf2、NQO1、HO-1、Bcl-2、Bax、caspase-3 和 caspase-9 蛋白的表达。这些数据表明，CA 通过调节 PI3K/Akt 和 Nrf2 信号通路对 APAP 诱导的肝毒性具有保护作用。
