HDAC1 expression is positively correlated with NADPH oxidase 4-mediated oxidative stress in a mouse model of traumatic brain injury.

Accumulating evidence has demonstrated that histone deacetylase 1 (HDAC1) expression is statistically correlated with the severity of traumatic brain injury (TBI). However, the specific role of HDAC1 in the occurrence and development of TBI remains unclear. The lateral fluid percussion injury (LFPI) was used to conduct TBI mouse model in C57BL/6J and C57BL/6J-Hdac1 em1cyagen mice. Western blot and qRT-PCR were performed to estimate the expression of HDAC1 and nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) in brain tissues. Modified neurological severity score (mNSS) and brain water content were analyzed to detect the neurological deficit. Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH) were used to detect the oxidative stress. Oxidative stresses, HDAC1, and NOX4 expression were upregulated in the lesioned cortices tissues after TBI. HDAC1 protein expression was positively correlated with the NOX4 in TBI mouse. Hdac1 knockout attenuated brain edema and neurological dysfunction caused by TBI in mice. Hdac1 knockout inhibited the expressions of NOX4 induced by TBI and attenuated TBI-induced oxidative stress. HDAC1 expression is positively correlated with to NOX4-mediated oxidative stress in a TBI mouse model. NEW & NOTEWORTHY Traumatic brain injury causes increased oxidative stresses, histone deacetylase 1, and nicotinamide adenine dinucleotide phosphate oxidase 4 expression. Hdac1 knockout could attenuate the brain damage caused by traumatic brain injury. The results suggest that histone deacetylase 1 may be a therapeutic target for the treatment of traumatic brain injury.