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.
Molecules. 2024 Mar 20;29(6):1384. doi: 10.3390/molecules29061384.
Que Zui tea (QT) is an important herbal tea in the diet of the 'Yi' people, an ethnic group in China, and it has shown significant antioxidant, anti-inflammatory, and hepatoprotective effects in vitro. This study aims to explore the protective effects of the aqueous-ethanol extract (QE) taken from QT against ᴅ-galactose (ᴅ-gal)-induced oxidative stress damage in mice and its potential mechanisms. QE was identified as UHPLC-HRMS/MS for its chemical composition and possible bioactive substances. Thus, QE is rich in phenolic and flavonoid compounds. Twelve compounds were identified, the main components of which were chlorogenic acid, quinic acid, and 6'--caffeoylarbutin. Histopathological and biochemical analysis revealed that QE significantly alleviated brain, liver, and kidney damage in ᴅ-gal-treated mice. Moreover, QE remarkably attenuated oxidative stress by activating the Nrf2/HO-1 pathway to increase the expression of antioxidant indexes, including GSH, GSH-Px, CAT, SOD, and T-AOC. In addition, QE administration could inhibit the IL-1β and IL-6 levels, which suppress the inflammatory response. QE could noticeably alleviate apoptosis by inhibiting the expressions of Caspase-3 and Bax proteins in the brains, livers, and kidneys of mice. The anti-apoptosis mechanism may be related to the upregulation of the SIRT1 protein and the downregulation of the p53 protein induced by QE in the brain, liver, and kidney tissues of mice. Molecular docking analysis demonstrated that the main components of QE, 6'--caffeoylarbutin, chlorogenic acid, quinic acid, and robustaside A, had good binding ability with Nrf2 and SIRT1 proteins. The present study indicated that QE could alleviate ᴅ-gal-induced brain, liver and kidney damage in mice by inhibiting the oxidative stress and cell apoptosis; additionally, the potential mechanism may be associated with the SIRT1/Nrf2 signaling pathway.
雀嘴茶（QT）是中国彝族饮食中一种重要的茶饮，体外研究表明其具有显著的抗氧化、抗炎和保肝作用。本研究旨在探讨 QT 的水醇提物（QE）对氯化半乳糖（ᴅ-gal）诱导的小鼠氧化应激损伤的保护作用及其潜在机制。QE 通过 UHPLC-HRMS/MS 进行了化学成分鉴定和可能的生物活性物质分析，结果表明 QE 富含酚类和黄酮类化合物。鉴定出 12 种化合物，主要成分为绿原酸、奎宁酸和 6'--咖啡酰基卢丁。组织病理学和生化分析表明，QE 可显著减轻氯化半乳糖处理小鼠的脑、肝和肾损伤。此外，QE 通过激活 Nrf2/HO-1 通路显著减轻氧化应激，增加抗氧化指标的表达，包括 GSH、GSH-Px、CAT、SOD 和 T-AOC。此外，QE 给药可通过抑制白细胞介素-1β（IL-1β）和白细胞介素-6（IL-6）水平抑制炎症反应。QE 可通过抑制小鼠脑、肝和肾组织中 Caspase-3 和 Bax 蛋白的表达明显抑制细胞凋亡。抗凋亡机制可能与 QE 上调脑、肝和肾组织中 SIRT1 蛋白和下调 p53 蛋白有关。分子对接分析表明，QE 的主要成分 6'--咖啡酰基卢丁、绿原酸、奎宁酸和罗望子苷 A 与 Nrf2 和 SIRT1 蛋白具有良好的结合能力。本研究表明，QE 可通过抑制氧化应激和细胞凋亡缓解氯化半乳糖诱导的小鼠脑、肝和肾损伤，其潜在机制可能与 SIRT1/Nrf2 信号通路有关。
