Regular Exercise with Panax Ginseng Supplementation Attenuates Arsenic-Induced Muscular Weakness and Neurobehavioral Changes in Mice.

Abstract

Arsenic (As) contamination of groundwater in some parts of Bangladesh has become a major threat to human health. Chronic exposure to As leads to anxiety development, memory impairment, and muscle weakness in humans and experimental animals. Panax ginseng (PG) is an herb utilized for multiple health-related applications. Furthermore, regular exercise (Ex) can reduce the risk of various diseases, and is also effective against heavy metal-associated neurotoxicity. Swiss albino mice were divided into five groups (n = 6) to evaluate the protective effects of Ex and PG (50 mg/kg body weight) supplementation against As-induced (10 mg/kg body weight) muscular weakness and neurobehavioral Changes for 60 days. Mice exposed to As showed weaker muscular strength, impaired memory and increased anxiety-like behavior along with the alteration of biochemical parameters related muscular weakness and neurobehavioral changes compared to control mice. However, As + Ex + PG-exposed mice showed significantly (p < 0.05) better performances in all behavioral tests compared to mice exposed to As alone. Additionally, compared to As-exposed mice, As + Ex + PG-exposed mice showed significantly improved (p < 0.05) activity of acetylcholinesterase (AChE), butyrylcholinesterase (BChE), superoxide dismutase (SOD), and reduced glutathione reductase (rGR) in brain, while serum levels of lactate dehydrogenase (LDH) and creatine kinase (CK) were reduced. Furthermore, levels of nuclear factor erythroid 2-related factor-2 (Nrf2), heme oxygenase-1 (HO-1), and interleukin-10 (IL-10) levels were increased, while interleukin-6 (IL-6) levels were decreased in brain tissue of As + Ex + PG-exposed mice compared to As-exposed mice. The results of this study suggest that Ex with PG supplementation can attenuate As-induced muscle weakness, cognitive disorder and anxiety development, possibly through the up-regulation of the Nrf2-HO-1 pathway in the As-exposure mice.