雀嘴茶中的6'-O-Caffeoylarbutin通过增强抗氧化能力和调节PI3K信号通路改善对乙酰氨基酚诱导的肝损伤,Food & Function

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雀嘴茶中的6'-O-Caffeoylarbutin通过增强抗氧化能力和调节PI3K信号通路改善对乙酰氨基酚诱导的肝损伤
Food & Function ( IF 5.1 ) Pub Date : 2022-04-06 , DOI: 10.1039/d2fo00507g
Yong-Peng Wang ₁ , Yu-Dan Wang _{1,

2} , Ya-Ping Liu ₁ , Jian-Xin Cao ₁ , Mei-Lian Yang ₁ , Yi-Fen Wang ₃ , Afsar Khan ₄ , Tian-Rui Zhao ₁ , Gui-Guang Cheng ₁

Affiliation

雀嘴茶（QT）是我国传统的凉茶，具有显着的保肝作用。6'- O -Caffeoylarbutin (CA) 是 QT 中最丰富的化合物。然而，尚未研究 CA 的保肝作用。本研究旨在评估 CA在体内和体外对对乙酰氨基酚 (APAP) 诱导的肝毒性的保护作用。及其可能的潜在机制。在 APAP 诱导的 HepG-2 细胞中，CA 抑制细胞内 ROS 积累和细胞凋亡，并改善包括 SOD、CAT 和 GSH 在内的抗氧化剂的表达。在 APAP 给药的小鼠中，CA 预处理显着改善了血清和肝组织中的组织病理学损伤和炎症反应以及抗氧化酶活性。此外，免疫组织化学和免疫荧光测定结果显示，CA 显着减少了 ROS 的产生和细胞凋亡，并激活了肝脏中的抗氧化转录因子 Nrf2。同时，分子对接结果表明CA和PI3K的强结合力是由于具有活性位点残基的氢键和π键数量较多。值得注意的是，CA 预处理显着调节 PI3K、Akt、Nrf2、NQO1、APAP 处理的肝组织中的 HO-1、Bcl-2、Bax、caspase-3 和 caspase-9 蛋白。这些数据表明 CA 对 APAP 诱导的肝毒性具有保护作用通过调节 PI3K/Akt 和 Nrf2 信号通路。

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6′-O-Caffeoylarbutin from Que Zui tea ameliorates acetaminophen-induced liver injury via enhancing antioxidant ability and regulating the PI3K signaling pathway

Que Zui tea (QT), a traditional herbal tea in China, has a significant hepatoprotective effect. 6′-O-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 in vivo and in vitro 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 via regulating the PI3K/Akt and Nrf2 signaling pathway.

更新日期：2022-04-06

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