Hao Yiming, Li Yanfang, Liu Jie, Wang Ziyuan, Gao Boyan, Zhang Yaqiong, Wang Jing
China-Canada Joint Lab of Food Nutrition and Health (Beijing), Beijing Technology & Business University (BTBU), Beijing, China.
Institute of Food and Nutraceutical Science, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai, China.
Front Nutr. 2021 Apr 7;8:648973. doi: 10.3389/fnut.2021.648973. eCollection 2021.
cv. Fubaiju is a kind of widely consumed herb tea with multiple health benefits. The present study was aimed to evaluate the protective capacity of cv. Fubaiju hot-water extracts (CMs) against ARPE-19 cell oxidative damage. The results showed that pretreatment with 100 μg/mL CM could significantly reduce cell oxidative damage and apoptosis. Proapoptotic protein expression such as Bax, cleaved caspase-3, and cleaved poly(ADP-ribose) polymerase (PARP) was significantly decreased after CM addition, while the expression level of antioxidant enzymes including catalase, glutamate-cysteine ligase catalytic subunit (GCLc), superoxide dismutase 2 (SOD2), and NAD(P)H:quinone oxidoreductase 1 (NQO-1) was significantly promoted. Meanwhile, CM treatment upregulated Akt phosphorylation, nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation, and the expression level of antioxidant gene heme oxygenase-1 (HO-1) in a dose-dependent manner under oxidative stress. Knockdown of Nrf2 by targeted small interfering RNA (siRNA) alleviated CM-mediated HO-1 transcription and almost abolished CM-mediated protection against hydrogen peroxide (HO)-induced cell damage. Correspondingly, the protective effect of CM was dramatically blocked after interference with phosphatidylinositol 3-kinase (PI3K)/Akt inhibitor LY294002, indicating that the protective effect of CM on cell oxidative damage was attributed to PI3K/Akt-mediated Nrf2/HO-1 signaling pathway.
福白菊是一种广泛饮用的花草茶，具有多种健康益处。本研究旨在评估福白菊热水提取物（CMs）对ARPE - 19细胞氧化损伤的保护能力。结果表明，用100μg/mL的CM预处理可显著降低细胞氧化损伤和凋亡。添加CM后，促凋亡蛋白如Bax、裂解的半胱天冬酶 - 3和裂解的聚（ADP - 核糖）聚合酶（PARP）的表达显著降低，而包括过氧化氢酶、谷氨酸 - 半胱氨酸连接酶催化亚基（GCLc）、超氧化物歧化酶2（SOD2）和NAD（P）H：醌氧化还原酶1（NQO - 1）在内的抗氧化酶的表达水平显著升高。同时，在氧化应激条件下，CM处理以剂量依赖的方式上调Akt磷酸化、核因子红细胞2相关因子2（Nrf2）核转位以及抗氧化基因血红素加氧酶-1（HO - 1）的表达水平。通过靶向小干扰RNA（siRNA）敲低Nrf2可减轻CM介导的HO - 1转录，并几乎消除CM介导的对过氧化氢（H₂O₂）诱导的细胞损伤的保护作用。相应地，在用磷脂酰肌醇3激酶（PI3K）/Akt抑制剂LY294002干扰后，CM的保护作用被显著阻断，表明CM对细胞氧化损伤的保护作用归因于PI3K/Akt介导的Nrf2/HO - 1信号通路。
