Axonal injury induced by carbonylation of cytoskeletal brain proteins in rats after traumatic brain injury

Abstract

Objective To investigate the oxidative stress and cytoskeleton protein carbonylation in rat brains after different severities of traumatic brain injury (TBI). Methods Fluid percussion percussion device was used to establish the mild, severe and sham-operated Sprague-Dawley rat models (n=15); 24 h after that, enzyme linked immunosorbent assay was used to detect the levels of malondialdehyde (MDA) and glutathione (GSH), and Western blotting was employed to detect the cytoskeletal proteins (β- actin, β- tublin and glial fibrillary acidic [GFAP]) carbonylation levels; phosphorylated tau (p- tau) protein expressions were examined by Western blotting. Results The expression levels of MDA in mild TBI group and severe TBI group were (389.62±29.95) μmol/g and (642.50±37.56) μmol/g, respectively, which was significantly increased as compared with the MDA level ([233.94±25.08] μmol/g) in sham-operated group (P<0.05). The expression level of GSH in mild TBI group and severe TBI group was (352.10±37.75) μmol/g and (153.27 ±43.49) μmol/g, respectively, which was significantly decreased as compared with the GSH level ([492.48±41.43] μmol/g) in sham-operated group (P<0.05). The β- actin, β- tublin and GFAP proteincarbonylation levels (0.099±0.104, 0.194±0.114 and 0.643±0.037; 0.142±0.017, 0.290±0.029 and 0.902±0.021) and p- tau level (0.289±0.014 and 0.373±0.012) in mild TBI group and severe TBI group were significantly higher than those in sham- operated group (0.068 ± 0.017, 0.108 ± 0.016 and 0.673 ± 0.032; 0.185±0.009;P<0.05). Conclusions The oxidative stress and carbonylation of cytoskeleton proteins are significantly increased after TBI, and the expression levels are correlated with the severity of TBI. The carbonylation of cytoskeleton protein aggravates the axonal injury after TBI. Key words: Traumatic brain injury; Oxidative stress; Cytoskeletal protein; Carbonylation