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多糖通过ROS-Drp1信号通路减轻六价铬诱导的DF-1细胞凋亡。

Polysaccharides Alleviate Cr(VI)-Induced Apoptosis in DF-1 Cells via ROS-Drp1 Signal Pathway.

作者信息

Zhang Zhuanglong, Zheng Pimiao, Qi Changxi, Cui Yuehui, Qi Yijian, Xue Kun, Yan Guangwei, Liu Jianzhu

机构信息

College of Veterinary Medicine, Shandong Agricultural University, Tai'an 271018, China.

Research Center for Animal Disease Control Engineering, Shandong Agricultural University, Tai'an 271018, China.

出版信息

Life (Basel). 2022 Dec 19;12(12):2144. doi: 10.3390/life12122144.

Abstract

Hexavalent chromium (Cr(VI)) is a widespread heavy metal that has been identified as a human carcinogen, and acute or chronic exposure to Cr(VI) can cause organ damage. polysaccharide (PGPS) is a constituent extracted from the Chinese herb , which has various pharmacological effects. Therefore, the author investigated the role of PGPSt in Cr(VI)-induced apoptosis in chicken embryo fibroblast cell lines (DF-1 cells). Firstly, this study infected DF-1 cells using Cr(VI) to set up a model for cytotoxicity and then added PGPSt. Then, the intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and apoptosis rate were evaluated. The results showed that PGPSt could inhibit Cr(VI)-induced mitochondrial damage and increase the apoptosis rate. For further exploration of the mechanism of regulation of PGPSt, the ROS-Drp1 pathway was investigated. The antioxidant N-acetyl-L-cysteine (NAC) and mitochondrial division inhibitor 1(Mdivi-1) were added, respectively. The results showed that the NAC and Mdivi-1 restored abnormal mitochondrial fission and cell apoptosis. Thus, PGPSt can alleviate Cr(VI)-induced apoptosis of DF-1 cells through the ROS-Drp1 signaling pathway, which may suggest new research ideas for developing new drugs to alleviate Cr(VI) toxicity.

摘要

六价铬(Cr(VI))是一种广泛存在的重金属,已被确认为人类致癌物,急性或慢性接触Cr(VI)会导致器官损伤。 多糖(PGPS)是从一种中草药中提取的成分,具有多种药理作用。因此,作者研究了PGPSt在Cr(VI)诱导的鸡胚成纤维细胞系(DF-1细胞)凋亡中的作用。首先,本研究用Cr(VI)感染DF-1细胞以建立细胞毒性模型,然后添加PGPSt。然后,评估细胞内活性氧(ROS)、线粒体膜电位(MMP)和凋亡率。结果表明,PGPSt可以抑制Cr(VI)诱导的线粒体损伤并提高凋亡率。为了进一步探索PGPSt的调控机制,研究了ROS-Drp1途径。分别添加抗氧化剂N-乙酰-L-半胱氨酸(NAC)和线粒体分裂抑制剂1(Mdivi-1)。结果表明,NAC和Mdivi-1恢复了异常的线粒体分裂和细胞凋亡。因此,PGPSt可以通过ROS-Drp1信号通路减轻Cr(VI)诱导的DF-1细胞凋亡,这可能为开发减轻Cr(VI)毒性的新药提供新的研究思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0289/9788446/b9d5f1ced163/life-12-02144-g001.jpg

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