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新鲜辣椒中辣椒素类糖苷通过依赖的信号通路对过氧化氢诱导的HepG2细胞氧化应激的保护作用。

Protective Effects of Capsaicinoid Glucoside from Fresh Hot Peppers Against Hydrogen peroxide-induced Oxidative Stress in HepG2 Cells Through-dependent Signaling Pathway.

作者信息

Elkhedir Abdeen, Yahya Alsadig, Mansour Mohammed, Korin Ali, Albahi Amgad, Khalifa Ibrahim, Maqsood Sajid, Xu Xiaoyun

机构信息

College of Food Science and Technology, Huazhong Agricultural University, No. 1, Shuzishan Road, Wuhan, 8430070, China.

Agro-Industries, Industrial Research and Consultancy Centre (IRCC), Khartoum, Sudan.

出版信息

Plant Foods Hum Nutr. 2024 Dec 30;80(1):25. doi: 10.1007/s11130-024-01250-2.

DOI:10.1007/s11130-024-01250-2
PMID:39739134
Abstract

This study aimed to investigate the protective effect of a novel capsaicinoid glucoside (CG) against HO-induced oxidative stress in HepG2 cells and elucidate its underlying molecular mechanism. CG treatment significantly reduced HO-induced cell mortality and attenuated the production of lactate dehydrogenase and malondialdehyde in a dose-dependent manner. Moreover, CG drastically reduced the ROS levels 18.7, 37.4, and 43.8% at concentrations of 25, 50, and 100 µg/mL, respectively. while increased glutathione content and catalase activity. Most importantly, in silico analysis revealed that CG effectively interacted with each of TRPV1 and Nrf2 by H-bonds, π-π interactions, and hydrophobic forces without simulation fluctuations over 50 ns. TRP, LYS, THR, LEU, GLN, VAL, ILE, and TYR residues of the tested proteins were all involved in the interaction with CG. These findings suggested that CG could reduce HO-induced oxidative stress in HepG2 cells via TRPV1/Nrf2 pathway which could be validated in functional foods/supplements formulations.

摘要

本研究旨在探讨一种新型辣椒素类糖苷(CG)对H2O2诱导的HepG2细胞氧化应激的保护作用,并阐明其潜在的分子机制。CG处理显著降低了H2O2诱导的细胞死亡率,并以剂量依赖的方式减弱了乳酸脱氢酶和丙二醛的产生。此外,CG在浓度为25、50和100μg/mL时,分别使活性氧水平大幅降低了18.7%、37.4%和43.8%,同时增加了谷胱甘肽含量和过氧化氢酶活性。最重要的是,计算机模拟分析表明,CG通过氢键、π-π相互作用和疏水作用力与TRPV1和Nrf2有效相互作用,在50 ns以上无模拟波动。受试蛋白的TRP、LYS、THR、LEU、GLN、VAL、ILE和TYR残基均参与了与CG的相互作用。这些发现表明,CG可通过TRPV1/Nrf2途径减轻H2O2诱导的HepG2细胞氧化应激,这一途径可在功能性食品/补充剂配方中得到验证。

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