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没食子酰基增强儿茶素对RAW264.7细胞中脂多糖引发炎症的抑制活性。

The Galloyl Group Enhances the Inhibitory Activity of Catechins against LPS-Triggered Inflammation in RAW264.7 Cells.

作者信息

Peng Jinming, Chen Guangwei, Guo Shaoxin, Lin Ziyuan, Li Jun, Yang Wenhua, Xiao Gengsheng, Wang Qin

机构信息

Guangdong Key Laboratory of Science and Technology of Lingnan Specialty Food, Zhongkai University of Agriculture and Engineering, Guangzhou 510225, China.

Key Laboratory of Green Processing and Intelligent Manufacturing of Lingnan Specialty Food, Ministry of Agriculture, Zhongkai University of Agriculture and Engineering, Guangzhou 510225, China.

出版信息

Foods. 2024 Aug 21;13(16):2616. doi: 10.3390/foods13162616.

Abstract

The galloyl group in catechins was confirmed to be crucial for their health benefits. However, whether the catechins' galloyl group had a contribution to their anti-inflammation remains unclear. This study investigated the anti-inflammation properties and mechanisms of catechins in RAW264.7 cells by using ELISA, fluorometry, flow cytometer, Western blot, and molecular docking. Results showed that the galloyl group enhanced the inhibitory abilities of catechins on inflammatory cytokines (NO, PGE, IL-1β, and TNF-α) and ROS release in LPS-induced cells. This suppression was likely mediated by delaying cells from the G0/G1 to the S phase, blocking COX-2 and iNOS via the TLR4/MAPK/NF-κB pathway with PU.1 as an upstream target. The research proved that the existence of galloyl groups in catechins was indispensable for their anti-inflammatory capacities and offered a theoretical basis for the anti-inflammatory mechanism of galloylated catechins. Future research is needed to verify the anti-inflammatory effects of catechins in various sources of macrophages or the Caco-2/RAW264.7 cell co-culture system.

摘要

儿茶素中的没食子酰基被证实对其健康益处至关重要。然而,儿茶素的没食子酰基是否对其抗炎作用有贡献仍不清楚。本研究通过酶联免疫吸附测定(ELISA)、荧光测定法、流式细胞仪、蛋白质免疫印迹法和分子对接,研究了儿茶素在RAW264.7细胞中的抗炎特性和机制。结果表明,没食子酰基增强了儿茶素对脂多糖诱导的细胞中炎性细胞因子(一氧化氮、前列腺素E、白细胞介素-1β和肿瘤坏死因子-α)和活性氧释放的抑制能力。这种抑制作用可能是通过延迟细胞从G0/G1期进入S期,以PU.1作为上游靶点,经由Toll样受体4/丝裂原活化蛋白激酶/核因子-κB途径阻断环氧化酶-2和诱导型一氧化氮合酶来介导的。该研究证明,儿茶素中没食子酰基的存在对其抗炎能力不可或缺,并为没食子酰化儿茶素的抗炎机制提供了理论依据。未来需要进一步研究以验证儿茶素在各种来源巨噬细胞或Caco-2/RAW264.7细胞共培养系统中的抗炎作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a33/11353959/d84399de1a8c/foods-13-02616-g001.jpg

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