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小麦胚芽肽缓解铅诱导 PC12 细胞氧化损伤的作用机制。

Mechanism of mitigating effect of wheat germ peptides on lead-induced oxidative damage in PC12 cells.

机构信息

Henan Engineering Technology Research Center of Food Processing and Circulation Safety Control, College of Food Science and Technology, Henan Agricultural University, 63# Agricultural Road, 450000 Zhengzhou, China.

Henan Engineering Technology Research Center of Food Processing and Circulation Safety Control, College of Food Science and Technology, Henan Agricultural University, 63# Agricultural Road, 450000 Zhengzhou, China.

出版信息

Ecotoxicol Environ Saf. 2022 Nov;246:114190. doi: 10.1016/j.ecoenv.2022.114190. Epub 2022 Oct 14.

DOI:10.1016/j.ecoenv.2022.114190
PMID:36252511
Abstract

It is well known that lead-induced neurotoxicity is closely related to oxidative stress. According to previous reports, wheat germ peptides (WGPs) isolated from wheat germ have been shown to have potent antioxidant capacity. This study hypothesized that WGPs could protect PC12 cells from lead-induced oxidative stress. Here, the protecting-efficacies of WGPs were investigated in PC12 cells that were pretreated with WGPs (200 μM, 4 h) and exposed to lead (10 μM, 24 h). The antioxidant capacity was assessed by cell viability, ROS, MDA, SOD, CAT, GR, GPx, GSH, and GSSG. The experimental results showed that WGP3, WGP8, and WGP9 could reverse the reduction of cell viability caused by lead exposure. Lead exposure causes oxidative stress by increasing the levels of ROS and MDA. Moreover, the decrease in the levels of SOD, CAT, GPx, GR, and GSH/GSSG could be observed. However, WGP3, WGP8, and WGP9 can protect PC12 cells against lead-induced oxidative stress by reversing these phenomena. The protein expression of TXNIP, Keap1, and Nrf2 was characterized by western blotting, and the results illustrated that lead exposure up-regulated the expression of TXNIP and Keap1 and down-regulated the expression of Nrf2, and WGP3, WGP8, and WGP9 could improve the antioxidant capacity of PC12 cells by reversing this phenomenon. Therefore, the present study demonstrated that WGP3, WGP8, and WGP9 may protect against lead-induced oxidative stress in PC12 cells by regulating the TXNIP/Keap1/Nrf2 pathway.

摘要

众所周知,铅诱导的神经毒性与氧化应激密切相关。根据以往的报告,从麦芽中分离出的麦芽肽(WGPs)已被证明具有很强的抗氧化能力。本研究假设 WGPs 可以保护 PC12 细胞免受铅诱导的氧化应激。在这里,研究了 WGPs 在先用 WGPs(200μM,4h)预处理然后暴露于铅(10μM,24h)的 PC12 细胞中的保护作用。通过细胞活力、ROS、MDA、SOD、CAT、GR、GPx、GSH 和 GSSG 评估抗氧化能力。实验结果表明,WGPs3、WGPs8 和 WGPs9 可以逆转铅暴露引起的细胞活力下降。铅暴露通过增加 ROS 和 MDA 的水平引起氧化应激。此外,还观察到 SOD、CAT、GPx、GR 和 GSH/GSSG 水平下降。然而,WGPs3、WGPs8 和 WGPs9 可以通过逆转这些现象来保护 PC12 细胞免受铅诱导的氧化应激。通过 Western blot 分析了 TXNIP、Keap1 和 Nrf2 的蛋白表达,结果表明,铅暴露上调了 TXNIP 和 Keap1 的表达,下调了 Nrf2 的表达,WGPs3、WGPs8 和 WGPs9 可以通过逆转这种现象来提高 PC12 细胞的抗氧化能力。因此,本研究表明,WGPs3、WGPs8 和 WGPs9 可能通过调节 TXNIP/Keap1/Nrf2 通路来保护 PC12 细胞免受铅诱导的氧化应激。

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