Alleviating Effect of Lipid Phytochemicals in Seed Oil (Brassica napus L.) on Oxidative Stress Injury Induced by H2O2 in HepG2 Cells via Keap1/Nrf2/ARE Signaling Pathway

文献类型： 外文期刊

第一作者： Peng, Simin

作者： Peng, Simin;Lin, Qian;Peng, Simin;Liao, Luyan;Deng, Huiqing;Wu, Weiguo;Liu, Xudong;Lin, Qian

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关键词： dietary phytochemicals; lipid phytochemicals; Brassica napus L.; central composite design; oxidative stress; Keap1/Nrf2

期刊名称：NUTRIENTS （ 影响因子：5.0； 五年影响因子：6.0 ）

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年卷期： 2024 年 16 卷 17 期

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收录情况： SCI

摘要： alpha-tocopherol (alpha-T), beta-sitosterol (beta-S), canolol (CA), and sinapic acid (SA) are the four main endogenous lipid phytochemicals (LP) found in Brassica napus L. seed oil, which possess the bioactivity to prevent the risk of several chronic diseases via antioxidant-associated mechanisms. Discovering the enhancer effects or synergies between LP is valuable for resisting oxidative stress and improving health benefits. The objectives of this study were to identify a potentially efficacious LP combination by central composite design (CCD) and cellular antioxidant activity (CAA) and to investigate its protective effect and potential mechanisms against H2O2-induced oxidative damage in HepG2 cells. Our results indicated that the optimal concentration of LP combination was alpha-T 10 mu M, beta-S 20 mu M, SA 125 mu M, and CA 125 mu M, respectively, and its CAA value at the optimal condition was 10.782 mu mol QE/100 g. At this concentration, LP combination exerted a greater amelioration effect on H2O2-induced HepG2 cell injury than either antioxidant (tea polyphenols or magnolol) alone. LP combination could reduce the cell apoptosis rate induced by H2O2, lowered to 10.06%, and could alleviate the degree of oxidative damage to cells (ROS down arrow), lipids (MDA down arrow), proteins (PC down arrow), and DNA (8-OHdG down arrow). Additionally, LP combination enhanced the antioxidant enzyme activities (SOD, CAT, GPX, and HO-1), as well as the T-AOC, and increased the GSH level in HepG2 cells. Furthermore, LP combination markedly upregulated the expression of Nrf2 and its associated antioxidant proteins. It also increased the expression levels of Nrf2 downstream antioxidant target gene (HO-1, SOD-1, MnSOD, CAT, GPX-1, and GPX-4) and downregulated the mRNA expression levels of Keap1. The oxidative-stress-induced formation of the Keap1/Nrf2 complex in the cytoplasm was significantly blocked by LP treatment. These results indicate that LP combination protected HepG2 cells from oxidative stress through a mechanism involving the activation of the Keap1/Nrf2/ARE signaling pathways.

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