Chronic cigarette smoke exposure enhances brain-derived neurotrophic factor expression in rats with traumatic brain injury

The involvement of brain-derived neurotrophic factor (BDNF) in regulating neuronal survival during neuron differentiation, growth, and maturation, and during the regeneration of injured nerve cells, has already been documented. In experimental Parkinson’s disease, chronic exposure to cigarette smoke increased BDNF levels and survival of dopaminergic neurons. BDNF is also elevated in traumatic brain injury (TBI), where it is potentially involved in post-injury repair and regeneration. The aim of this study was to investigate the effects of chronic exposure to cigarette smoke on BDNF expression and apoptosis in rats with TBI. Three groups of rats were compared: rats with TBI after chronic exposure to cigarette smoke, rats with TBI and no exposure to cigarette smoke, and sham-operated rats. BDNF mRNA expression in the hippocampus increased from 2 to 24 h after TBI, and chronic exposure to cigarette smoke upregulated TBI-induced BDNF mRNA elevation at 0, 2, 4, 12, and 24 h after head injury. The BDNF protein levels generally corresponded to the mRNA levels in the hippocampal region. Compared to the TBI group without smoke exposure, chronic cigarette smoke exposure in rats inhibited the decrease of the Bcl-2/Bax ratio and reduced P53 expression and apoptosis 24 h after TBI. In addition, neuronal damage in the parietal and cingulate cortex 7 days after TBI was less extensive in rats exposed to cigarette smoke. In conclusion, although chronic exposure to cigarette smoke is a risk factor for myocardial and pulmonary disease, cigarette smoke exposure increases BDNF expression after TBI and thereby can play a neuroprotective role.