Abstract: AIM: To explore the possible mechanism of the neuroprotective effect of compound decotion on traumatic brain injury model.METHODS: The traumatic brain injury rat model was induced by improved Feeneys fall weight method and divided into sham operation group, TBI model group and compound decotion treatment group, compound decotion treatment group rats were intragastrically administered with compound decotion at 10 g·kg^-1·d^-1. Sham operation group and TBI model group were treated with same dose of normal saline, twice per day for seven days. The brains were taken out at 24, 72 h and one week after injury, respectively. The morphological changes were observed by HE staining in the cerebral cortex. The NO and NOS concentration and neuronal nitric oxide synthase (nNOS) activity were detected by neurochemistry stain method. nNOS expression were detected by immunohistochemical method. nNOS-mRNA expression were detected by in situ hybridization.RESULTS: In TBI model group, the concentration of NO and NOS and the activity and expression of nNOS and the expression of nNOS- mRNA were markedly elevated at different degrees at different time point and especially 24 hours after injury and still higher than those of sham operation group one week after injury. However, compared with the TBI model group, the concentration of NO and NOS and the activity and expression of nNOS and the expression of nNOS-mRNA in compound decotion treatment group were obviously decreased and reach normal level one week after injury (P＜0.05).CONCLUSION: NO and nNOS play an important role in the pathophysiological process of TBI. Inhibition of activated NO and nNOS and mitigate secondary brain injury may represent a potential neuroprotective mechanism for the treatment of TBI with compound decotion.

Key words: Traumatic brain injury, Nitric oxide, Neuronal nitric oxide synthase