L-Cysteine augments microtubule-associated protein 2 levels and enhances antioxidant activity in rats following traumatic brain injury.

Abstract

l-Cysteine is a well-known sulfur-containing non-essential amino acid that can be oxidized to cysteine, which possesses a variety of pharmacological actions, including antioxidant and anti-inflammatory activities. Traumatic brain injury (TBI) is defined as a closed head injury that leads to temporary alterations in neural function and further leads to pathophysiological processes. In the present study, rats were categorized into sham, control, 100mg/kgl-cysteine, and 200mg/kgl-cysteine groups and then the levels of lipid peroxidation, reduced glutathione (GSH), catalase, superoxide dismutase (SOD), reactive oxygen species (ROS), and mRNA and protein expression of microtubule-associated protein 2 (MAP2) were determined. Following supplementation with l-cysteine, there were reductions in lipid peroxidation and ROS levels, whereas catalase, SOD, and GSH levels increased. Additionally, the mRNA expression of MAP2 in the control rats was drastically reduced by 67% compared to the sham rats. However, supplementation with 100mg/kg of l-cysteine and 200mg/kg of l-cysteine significantly increased MAP2 mRNA expression by 84.8% and 169.7%, respectively. Similarly, MAP2 protein expression was drastically reduced by 61% in control rats compared to sham rats, but supplementation with 100mg/kg of l-cysteine and 200mg/kg of l-cysteine significantly increased MAP2 protein expression by 41% and 94.9%, respectively. Taken together, these data suggest that supplementation with l-cysteine significantly reduced lipid peroxidation and ROS levels, but increased antioxidant levels and the mRNA and protein expression of MAP2 in rats following TBI.