Abstract
Alpha-Linolenic acid (ALA), an omega-3 polyunsaturated fatty acid, is extracted from plant sources and has been shown to be one of the anti-inflammatory and antioxidant agents. Herein, we revealed the molecular mechanism underlying the anti-inflammatory and antioxidant potential of (ALA), against cadmium in the adult mouse brain. We evaluated the neuroprotective effect of ALA (60 mg/kg per oral for 6 weeks) against CdCl2 (5 mg/kg)-induced oxidative stress, neuroinflammation, and neuronal apoptosis. According to our findings, ALA markedly reduced ROS production and nitric oxide synthase 2 (NOS2) and enhanced the expression of nuclear factor-2 erythroid-2 (Nrf-2) and heme oxygenase-1 (HO-1) in mice treated with CdCl2. Most importantly, the molecular docking study revealed that ALA allosterically decreases the overexpression of c-Jun N-terminal kinase (JNK) activity and inhibited the detrimental effect against CdCl2. Moreover, ALA suppressed CdCl2-induced glial fibrillary acidic protein (GFAP), nuclear factor-kappa b (NF-κB), and interleukin-1β (IL-1β) in the mouse brain. Further, we also checked the pro- and anti-apoptotic proteins markers such as Bax, Bcl-2, and caspase-3, which were regulated in the cortex of ALA co-treated mouse brain. Overall, our study suggests that oral administration of ALA can impede oxidative stress, neuroinflammation, and increase neuronal apoptosis in the cortex of Cd-injected mouse brain.
Highlights
Heavy metals, including Cd, leads, and mercury-like metals, are widely distributed in nature without any nutritional importance
Alpha-Linolenic acid (ALA) Rescues Oxidative Stress by Improving Nuclear factor-2 erythroid-2 (Nrf2)/heme oxygenase-1 (HO-1) Signaling after Cd Administration in the Mouse Brain
The current study aimed to investigate the neuroprotective effect of ALA an omega3 polyunsaturated fatty acid against Cd-induced oxidative stress, neuroinflammation, increase neuronal apoptosis, and neurodegeneration after oral administration in the cortex
Summary
Heavy metals, including Cd, leads, and mercury-like metals, are widely distributed in nature without any nutritional importance. The main sources by which humans come across it in daily activities include automobiles and cigarette smoke [3,4]. Cd is aggregated in several human organs of the body including lungs, liver, stomach, and brain which destroy these organs structure and function [6,7,8]. Among these organs, the brain is the most sensitive organ and target for Cd-induced neurotoxicity, including oxidative stress, neuroinflammation, and neurodegeneration [2,9,10]. Several studies have reported that oxidative stress is mainly involved in the pathogenesis of Cd-induced neurodegeneration. Other studies have reported that reactive oxygen species (ROS) and lipid peroxidation (LPO)
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