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微囊藻毒素诱导氧化应激后,核因子 E2 相关因子 2 和肌动蛋白腱膜纤维肉瘤 K 介导褶皱臂尾轮虫谷胱甘肽过氧化物酶的调节。

Nuclear factor E2-associated factor 2 and musculoaponeurotic fibrosarcoma K mediate regulation glutathione peroxidase of Cristaria plicata after microcystin-induced oxidative stress.

机构信息

College of Life Science, Education Ministry Key Laboratory of Poyang Lake Environment and Resource Utilization, Nanchang University, Nanchang 330031, China.

College of Life Science, Education Ministry Key Laboratory of Poyang Lake Environment and Resource Utilization, Nanchang University, Nanchang 330031, China.

出版信息

Comp Biochem Physiol C Toxicol Pharmacol. 2023 Nov;273:109742. doi: 10.1016/j.cbpc.2023.109742. Epub 2023 Sep 7.

Abstract

Nuclear factor E2-associated factor 2 (Nrf2)/Antioxidant Response Element (ARE) signaling pathway is an endogenous antioxidant pathway that protects cells from oxidative damage. This pathway is triggered when aquatic organisms are exposed to environmental toxicants. In this study, CpMafK (musculoaponeurotic fibrosarcoma K of Cristaria plicata) mRNA expression in hepatopancreas and gills were up regulated after Cristaria plicata (C. plicata) was exposed to microcystin (MC), which showed that CpMafK protected C. plicata from MC. After MC treatment and CpNrf2 (Nrf2 of Cristaria plicata) knockdown, the mRNA expression of CpMafK was down regulated. After MC treatment and CpMafK knockdown, the mRNA expression of CpNrf2 was down regulated. Indicating that the expression of CpNrf2 was positively correlated with CpMafK. CpGPx (GPx of Cristaria plicata) mRNA was also down regulated with the down regulation of CpMafK and CpNrf2. CpGPx promoter contains a variety of transcription factor binding sites, including Nrf2, ARE elements, etc. Gel blocking experiments showed that CpNrf2/CpMafK heterodimers were bound to CpGPx promoters in vitro. Dual luciferase reporter assay showed that CpNrf2/CpMafK heterodimer negatively regulated CpGPx promoter in cells. In conclusion, Nrf2 and MafK mediate regulation of GPx play a crucial role in protecting bivalves from MC.

摘要

核因子 E2 相关因子 2(Nrf2)/抗氧化反应元件(ARE)信号通路是一种内源性抗氧化途径,可保护细胞免受氧化损伤。当水生生物暴露于环境毒物时,该途径会被触发。在本研究中,在褶纹冠蚌(Cristaria plicata)暴露于微囊藻毒素(MC)后,其肝胰腺和鳃中的 CpMafK(musculoaponeurotic fibrosarcoma K of Cristaria plicata)mRNA 表达上调,表明 CpMafK 可保护褶纹冠蚌免受 MC 侵害。在 MC 处理和 CpNrf2(褶纹冠蚌的 Nrf2)敲低后,CpMafK 的 mRNA 表达下调。在 MC 处理和 CpMafK 敲低后,CpNrf2 的 mRNA 表达下调。表明 CpNrf2 的表达与 CpMafK 呈正相关。CpGPx(褶纹冠蚌的 GPx)mRNA 的表达也随着 CpMafK 和 CpNrf2 的下调而下调。CpGPx 启动子包含多种转录因子结合位点,包括 Nrf2、ARE 元件等。凝胶阻滞实验表明,CpNrf2/CpMafK 异二聚体在体外与 CpGPx 启动子结合。双荧光素酶报告基因检测显示,CpNrf2/CpMafK 异二聚体在细胞内负调控 CpGPx 启动子。综上所述,Nrf2 和 MafK 介导的 GPx 调节在保护双壳类动物免受 MC 侵害方面发挥着关键作用。

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