Docosahexaenoic Acid Protects against 1-Bromopropane Induced Cognitive Deficits in Rats involving in GSK-3β Activation and Oxidative Stress InhibitionJunlin Yang1, Hua Yuan2, Lulu Jiang1, Ying Guo1, Zengjin Wang1, Keqin Xie1 and Xiulan Zhao1*
- *Corresponding Author:
- Xiulan Zhao
Institute of Toxicology, School of Public Health
Shandong University, Jinan, Shandong Province, 250012, China
Tel: +86 531 88382132
E-mail: [email protected]
Received date: September 23, 2016; Accepted date: November 01, 2016; Published date: November 08, 2016
Citation: Yang J, Yuan H, Jiang L, Guo Y, Wang Z, et al. (2016) Docosahexaenoic Acid Protects against 1-Bromopropane Induced Cognitive Deficits in Rats involving in GSK-3β Activation and Oxidative Stress Inhibition. J Alzheimers Dis Parkinsonism 6:282. doi:10.4172/2161-0460.1000282
Copyright: © 2016 Yang J, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
A number of organic solvent are known to be neurotoxic substance, which can cause neurotoxicological effects in humans. 1-Bromopropane (1-BP) is an alternative to ozone-depleting solvent that widely used in industrial production. Occupational exposure to 1-BP becomes a major health concern due to its neurotoxicity displayed in animals and humans. Docosahexaenoic acid (DHA), long chain n-3 polyunsaturated fatty acids (PUFA) and the main component of fish oil, is essential for normal neurological development and displays potent neuroprotective capacity. Here we investigate the protective effects and underlying mechanisms of DHA against 1-BP-induced deficits of spatial learning and memory ability in rats. Cognitive performance was assessed by Morris Water Maze test (MWM). Neuronal injury was determined by Nissl staining and TUNEL staining. The apoptosis-related proteins, including cleaved caspase-3, Bcl-2 and Bax, and proteins modified by 4-hydroxy-2-nonenal (4-HNE) or acrolein, in the brain were determined by Western blot. The inactive glycogen synthase kinase-3β (GSK-3β) in the brain of rats was also detected by specific antibody. Exposure to 1-BP resulted in learning deficits and memory loss of rats, neuronal apoptosis in the hippocampus cornu ammonis 3 (CA3) and prefrontal cortex, accompanied with significant GSK-3β inhibition by phosphorylation. Importantly, we found that pre-treatment with DHA significantly improved MWM performances of rats intoxicated with 1-BP, as well as the abrogation of neuron loss, alleviation of redox unbalance and GSK-3β activation in the brain. Our findings suggested that DHA supplementation would be a promising intervention for the central neurotoxicity of 1-BP, which might be correlated with oxidative stress and GSK-3β inhibition.