Effect Of NOS On The Neuronal Apoptosis After Traumatic Brain Injury In Rats

[Background] There exit primary pathological changes and secondary pathological changes after traumatic brain injury(TBI). The present study proved that apoptosis is responsible for the secondary pathological changes after TBI. Both apoptosis and anti-apoptosis process which control the neuronal apoptosis initiated after brain injury. Both Fas gene and Bcl-2 gene are involved in the process of neuronal apoptosis. The expression of Fas gene could promote neuronal apoptosis, but the expression of Bcl-2 gene has the opposite effect. NO/NOS system plays a great role in neuronal apoptosis after TBI. NOS which promotes the synthesis of NO includes neuronal NOS (nNOS) and inducible NOS (iNOS). Although it has been proved that NO could elicit the neuronal apoptosis, the effects of nNOS and iNOS on the neuronal apoptosis and the roles of Bcl-2 and Fas in the function of nNOS and iNOS after TBI are unknown.[Aim] To investigate the effects of nNOS and iNOS on the neuronal apoptosis after TBI and the underlying mechanism.[Methods] 330 male SD rats were randomly divided into 5 groups: Control group, fake operation group, trauma group, 7-NI (7-Nitroindazole, the inhibitor of nNOS) group (25mg/Kg/d, ip) and AG(Aminoguanidine, the inhibitor of iNOS) group (100mg/Kg/d, ip). The fake operation group, trauma group, 7-NI group and AG group were divided into 8 subgroups according to time phase after brain injury, which was 3h, 6h, 12h, 24h, 48h, 72h, 168h and 336h. Each subgroup and control group had 10 rats. The injury of hippocampal CA1 after brain injury was observed by using HE staining. Marmarou model of severe brain injury in rats were used to investigate the neuronal apoptosis, the expression of Bcl-2 and Fas in the hippocampal CA1 region at each time point after brain injury by TUNEL in situ and immunohistochemistry. The injury of hippocampal CA1 after brain injury was observed by using HE staining.