EMAIL THIS PAGE TO A FRIEND

Experimental and therapeutic medicine

Inhibition of cytoskeletal protein carbonylation may protect against oxidative damage in traumatic brain injury.


PMID 28101189

Abstract

Oxidative stress is the principal factor in traumatic brain injury (TBI) that initiates protracted neuronal dysfunction and remodeling. Cytoskeletal proteins are known to be carbonylated under oxidative stress; however, the complex molecular and cellular mechanisms of cytoskeletal protein carbonylation remain poorly understood. In the present study, the expression levels of glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) were investigated in PC12 cells treated with H