文献类型：期刊文献

英文题名：

Potentilla anserine L.& nbsp;polysaccharide protects against cadmium-induced neurotoxicity

作者：Cheng, Ju[1,5];Zhao, Lixia[2,3,5];Liu, Di[4,5];Shen, Rong[3,5];Bai, Decheng[2,5]

第一作者：Cheng, Ju

通信作者：Cheng, J[1]

机构：[1]Lanzhou Univ, Inst Genet, Sch Basic Med Sci, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Sch nursing, Lanzhou 730000, Peoples R China;[3]Lanzhou Univ, Lab Ctr Med Sci, Sch Basic Med Sci, Lanzhou 730000, Peoples R China;[4]Gansu Univ Polit Sci & Law, Key Lab Evidence Sci Tech Res & Applicat Gansu Pro, Lanzhou 730000, Peoples R China;[5]Lanzhou Univ, Inst Anat & Histol, Sch Basic Med Sci, Lanzhou 730000, Peoples R China

第一机构：Lanzhou Univ, Inst Genet, Sch Basic Med Sci, Lanzhou 730000, Peoples R China

通信机构：[1]corresponding author), Lanzhou Univ, Inst Genet, Sch Basic Med Sci, Lanzhou 730000, Peoples R China.

年份：2022

卷号：90

外文期刊名：ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY

收录：;Scopus(收录号：2-s2.0-85123071168);WOS:【SCI-EXPANDED(收录号:WOS:000788239300003)】；

基金：The work was supported by the Natural Science Foundation of Gansu Province of China (No. 20JR10RA600) and the Key Scientific Projects of Gansu University of Political Science and Law (No. GZF2020XZD15) . We would like to express our sincere thanks to Professor Xiaoyun Zhang for her help in the preparation of Potentilla anserina L. polysaccharide.

语种：英文

外文关键词：Cadmium; Neurotoxicity; Polysaccharide; N2a cells; SH-SY5Y cells; Cerebral cortex

摘要：Cadmium is a toxic metal that can damage the brain and other organs. This study aimed to explore the protective effects of Potentilla anserine L. polysaccharide (PAP) against CdCl2-induced neurotoxicity in N2a and SH-SY5Y cells and in the cerebral cortex of BALB/c mice. In addition, we aimed to identify the potential mechanisms underlying these protective effects. Relative to CdCl2 treatment alone, pretreatment with PAP prevented the reduction in cell viability evoked by CdCl2, decreased rates of apoptosis, promoted calcium homeostasis, decreased ROS accumulation, increased mitochondrial membrane potential, inhibited cytochrome C and AIF release, and prevented the cleavage of caspase-3 and PARP. In addition, PAP significantly decreased the CdCl2- induced phosphorylation of CaMKII, Akt, and mTOR. In conclusion, PAP represents a potential therapeutic agent for the treatment of Cd-induced neurotoxicity, functioning in part via attenuating the activation of the mitochondrial apoptosis pathway and the Ca2+-CaMKII-dependent Akt/mTOR pathway.