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硒化壳聚糖通过 JNK/SAPK 信号通路保护猪子宫内膜上皮细胞免受玉米赤霉烯酮诱导的凋亡。

Selenium-Chitosan Protects Porcine Endometrial Epithelial Cells from Zearalenone-induced Apoptosis via the JNK/SAPK Signaling Pathway.

机构信息

Tianjin Key Laboratory of Agricultural Animal Breeding and Healthy Husbandry, College of Animal Science and Veterinary Medicine, Tianjin Agricultural University, Xiqing District, No 22 Jinjing Road, Tianjin, 300392, China.

College of Veterinary Medicine, Qingdao Agricultural University, Chengyang District, No 700 Changcheng Road, Qingdao, 266109, China.

出版信息

Biol Trace Elem Res. 2024 May;202(5):2075-2084. doi: 10.1007/s12011-023-03816-8. Epub 2023 Aug 23.

DOI:10.1007/s12011-023-03816-8
PMID:37610602
Abstract

This study was designed to assess whether selenium-chitosan (Se-CTS) can protect porcine endometrial epithelial cells (PEECs) against damage and apoptosis induced by zearalenone (ZEA) via modulating the JNK/SAPK signaling pathway. The cell cycle, mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and apoptosis rates of porcine endometrial epithelial cells were determined, as well as the expression levels of genes related to the SAPK/JNK signaling pathway. The results showed that 3.0 µmol/L Se-CTS decreased the percentage of ZEA-induced G1 phase in PEECs (P < 0.01), whereas 1.5 and 3.0 µmol/L Se-CTS increased the percentage of ZEA-induced percentage of G2 phase of PEECs (P < 0.01). Further, Se-CTS at 1.5 and 3.0 µmol/L improved the ZEA-induced decrease in MMP (P < 0.01), whereas Se-CTS at 0.5, 1.5, and 3.0 µmol/L reduced the increase in ROS levels and apoptosis rate induced by ZEA in PEECs (P < 0.01 or P < 0.05). Furthermore, 3.0 µmol/L Se-CTS ameliorated the increase in the expression of c-Jun N-terminal kinase (JNK), apoptosis signal-regulated kinase (ASK1), and c-Jun induced by ZEA (P < 0.01) and the reduction in mitogen-activated protein kinase kinase 4 (MKK4) and protein 53 (p53) expression (P < 0.01), while 1.5 µmol/L Se-CTS improved the expression of ASK1 and c-Jun induced by ZEA (P < 0.05). The results proved that Se-CTS alleviates ZEA-induced cell cycle stagnation, cell mitochondrial damage, and cell apoptosis via decreasing ZEA-produced ROS and modulating the JNK/SAPK signaling pathway.

摘要

本研究旨在评估硒壳聚糖(Se-CTS)是否可以通过调节 JNK/SAPK 信号通路来保护猪子宫内膜上皮细胞(PEECs)免受玉米赤霉烯酮(ZEA)诱导的损伤和凋亡。测定了猪子宫内膜上皮细胞的细胞周期、线粒体膜电位(MMP)、活性氧(ROS)和凋亡率,以及与 SAPK/JNK 信号通路相关的基因表达水平。结果表明,3.0 μmol/L Se-CTS 降低了 ZEA 诱导的 PEECs G1 期的比例(P < 0.01),而 1.5 和 3.0 μmol/L Se-CTS 增加了 ZEA 诱导的 PEECs G2 期的比例(P < 0.01)。此外,1.5 和 3.0 μmol/L 的 Se-CTS 改善了 ZEA 诱导的 MMP 降低(P < 0.01),而 0.5、1.5 和 3.0 μmol/L 的 Se-CTS 降低了 ZEA 诱导的 ROS 水平升高和 PEECs 凋亡率(P < 0.01 或 P < 0.05)。此外,3.0 μmol/L Se-CTS 改善了 ZEA 诱导的 c-Jun N 末端激酶(JNK)、凋亡信号调节激酶(ASK1)和 c-Jun 表达增加(P < 0.01)以及丝裂原激活蛋白激酶激酶 4(MKK4)和蛋白 53(p53)表达减少(P < 0.01),而 1.5 μmol/L Se-CTS 改善了 ZEA 诱导的 ASK1 和 c-Jun 表达(P < 0.05)。结果证明,Se-CTS 通过减少 ZEA 产生的 ROS 和调节 JNK/SAPK 信号通路来减轻 ZEA 诱导的细胞周期停滞、细胞线粒体损伤和细胞凋亡。

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本文引用的文献

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Toxins (Basel). 2022 Nov 3;14(11):758. doi: 10.3390/toxins14110758.
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Role of PI3K/Akt-Mediated Nrf2/HO-1 Signaling Pathway in Resveratrol Alleviation of Zearalenone-Induced Oxidative Stress and Apoptosis in TM4 Cells.白藜芦醇通过 PI3K/Akt 介导的 Nrf2/HO-1 信号通路减轻玉米赤霉烯酮诱导的 TM4 细胞氧化应激和凋亡
Toxins (Basel). 2022 Oct 26;14(11):733. doi: 10.3390/toxins14110733.
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Selenium-chitosan alleviates the toxic effects of Zearalenone on antioxidant and immune function in mice.
硒-壳聚糖减轻玉米赤霉烯酮对小鼠抗氧化和免疫功能的毒性作用。
Front Vet Sci. 2022 Oct 6;9:1036104. doi: 10.3389/fvets.2022.1036104. eCollection 2022.
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Zearalenone Promotes LPS-Induced Oxidative Stress, Endoplasmic Reticulum Stress, and Accelerates Bovine Mammary Epithelial Cell Apoptosis.玉米赤霉烯酮促进 LPS 诱导的氧化应激、内质网应激,并加速奶牛乳腺上皮细胞凋亡。
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