Curcumin Ameliorates Copper-Induced Neurotoxicity Through Inhibiting Oxidative Stress and Mitochondrial Apoptosis in SH-
- PDF / 1,757,550 Bytes
- 12 Pages / 595.276 x 790.866 pts Page_size
- 89 Downloads / 237 Views
ORIGINAL PAPER
Curcumin Ameliorates Copper-Induced Neurotoxicity Through Inhibiting Oxidative Stress and Mitochondrial Apoptosis in SH-SY5Y Cells Biao Xiang1 · Daowen Li2 · Yiqiang Chen3 · Meng Li1 · Yuan Zhang1 · Tun Sun1 · Shusheng Tang1 Received: 2 April 2020 / Revised: 5 November 2020 / Accepted: 10 November 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Impaired homeostasis of copper has been linked to different pathophysiological mechanisms in neurodegenerative diseases and oxidative injury has been proposed as the main mechanism. This study aims to use curcumin, a widely used antioxidative and anti-apoptotic agent, to exert the neuroprotective effect against copper in vitro and illuminate the underlying mechanism. The effect of curcumin was examined by using a cell counting kit-8 assay, flow cytometry, immunofluorescence, spectrophotometer, and western blot. Results revealed that after pretreatment with curcumin for 3 h, copper-induced toxicity and apoptosis show a significant decline. Further experiments showed that curcumin not only decreased the production of ROS and MDA but also increased the activities of the ROS scavenging enzymes SOD and CAT. Moreover, curcumin treatment alleviated the decrease in mitochondrial membrane potential and the nuclear translocation of cytochrome c induced by copper. The protein levels of pro-caspase 3, pro-caspase 9, and PARP1 were up-regulated and the Bax/Bcl-2 ratio was down-regulated in the presence of curcumin. Taken together, our study demonstrates that curcumin has neuroprotective properties against copper in SH-SY5Y cells and the potential mechanisms might be related to oxidative stress and mitochondrial apoptosis. Keywords Curcumin · Copper · Reactive oxygen species · Mitochondrial · Apoptosis
Introduction Copper is an essential trace element, serving as structural and metabolic cofactors for metalloenzymes that involves in diverse cellular processes, including DNA modification, energy metabolism, antioxidant defense, and iron metabolism [1]. Pertinent to the brain, copper is indispensable for neuronal activities such as neurotransmission, * Shusheng Tang [email protected] 1
College of Veterinary Medicine, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, People’s Republic of China
2
Tianjin Key Laboratory of Agricultural Animal Breeding and Healthy Husbandry, College of Animal Science and Veterinary Medicine, Tianjin Agricultural University, Jinjing Road No.22, Xiqing District, Tianjin 300384, People’s Republic of China
3
State Key Laboratory of Animal Nutrition, China Agricultural University, No. 2 Yuanmingyuan West Road, Beijing 100193, People’s Republic of China
synaptogenesis, neurogenesis, neurite outgrowth, and neurotransmitter biosynthesis [2]. The disruption of copper homeostasis in the brain has consequently been related to several neurodegenerative disorders such as Wilson disease (WD), Parkinson’s, Huntington’s and Alzheimer’s disease. WD is the inherited multisystemic copp
Data Loading...
