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线粒体功能障碍导致来自海蜇 Cyanea capillata 的触须提取物在大鼠肾小管上皮 NRK-52E 细胞中诱导的细胞毒性。

Mitochondrial dysfunction contributes to the cytotoxicity induced by tentacle extract from the jellyfish Cyanea capillata in rat renal tubular epithelial NRK-52E cells.

机构信息

Department of Marine Biotechnology, Faculty of Naval Medicine, Second Military Medical University, Shanghai 200433, China.

出版信息

Toxicon. 2013 Nov;74:1-7. doi: 10.1016/j.toxicon.2013.07.020. Epub 2013 Aug 2.

Abstract

Our previous studies have shown that tentacle extract (TE) from the jellyfish Cyanea capillata could induce a delayed jellyfish envenomation syndrome with severe multiple organ dysfunctions, among which renal injury with tubular necrosis seemed to be most serious. So, in this study, we aimed to explore the toxic effect of TE on rat renal tubular epithelial NRK-52E cells. Based on the previous findings that TE could cause oxidative damage in erythrocytes, the effects of TE on cell oxidative stress conditions, including ROS production and lipid peroxidation, and mitochondrial dysfunction associated with cell death were investigated in NRK-52E cells. The results showed that TE caused cell morphological change and decreased cell viability through induction of apoptosis and necrosis in NRK-52E cells. Meanwhile, ROS overproduction and mitochondrial membrane potential decrease were found before the cell death occurred. It was concluded that TE could induce cytotoxicity, especially apoptosis and necrosis, in NRK-52E cells, and mitochondrial dysfunction and ROS overproduction might play important roles in the process of cell injury and death.

摘要

我们之前的研究表明,来自海月水母(Cyanea capillata)的触手提取物(TE)可诱发延迟性水母蜇伤综合征,并伴有严重的多器官功能障碍,其中肾小管坏死似乎最为严重。因此,在这项研究中,我们旨在探讨 TE 对大鼠肾小管上皮 NRK-52E 细胞的毒性作用。基于之前的研究结果,即 TE 可引起红细胞氧化损伤,我们研究了 TE 对 NRK-52E 细胞的细胞氧化应激状态的影响,包括 ROS 产生和脂质过氧化,以及与细胞死亡相关的线粒体功能障碍。结果表明,TE 通过诱导 NRK-52E 细胞凋亡和坏死导致细胞形态改变和细胞活力下降。同时,在细胞死亡发生之前,发现 ROS 过度产生和线粒体膜电位下降。由此得出结论,TE 可诱导 NRK-52E 细胞产生细胞毒性,尤其是凋亡和坏死,线粒体功能障碍和 ROS 过度产生可能在细胞损伤和死亡过程中发挥重要作用。

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