Abstract:【Abstract】 Objective To study the protective effects of pramipexole on neurological function in rats with craniocerebral injury. Methods 60 healthy adult SD rats were randomly divided into sham operation group, model group, lowdose pramipexole (0125 mg/Kg) group and highdose (025 mg/Kg) pramipexole group, with 15 rats in each group. Model group and pramipexole groups were fixed in Freeny's free fall frame to construct rat model of craniocerebral injury, and sham operation group was only given head trauma without hitting. After the model construction, pramipexole group was given the corresponding dose of pramipexole, and sham operation group and model group were intragastrically administered with the same volume of normal saline once a day for 14 d. The neurological function of each group was evaluated by mNSS scoring system on 1st d, 7th d and 14th d of treatment. Morris water maze test was performed at 9 to 13 d after operation, and the escape latency, platform frequency and residence time in the target quadrant were recorded in each group. The brain tissue of rats was taken for immunohistochemical staining at 15 d after operation, and the expression levels of cleavedcaspase3 and IL6 were analyzed. The protein expression levels of NFκB, MMP9 and VEGF in rat brain tissue were detected by western blot. Results There was no significant difference in mNSS score among the groups on the 1st d after treatment (P>005), but the mNSS score in pramipexole groups was significantly decreased on the 7th d and 14th d (P<005). Morris water maze results showed that the escape latency in pramipexole groups was significantly lower than that in model group, and platform frequency and time in the target quadrant were significantly higher than those in model group (P<005). Immunohistochemical staining showed that the expression levels of activated caspase3 protein and IL6 in pramipexole groups were significantly lower than those in model group. Western blot results showed that the protein expression levels of NFκB, MMP9 and VEGF in pramipexole groups were significantly higher than those in model group (P<005). Conclusion Pramipexole can inhibit cell apoptosis by decreasing the expression of inflammatory factor IL6 and apoptin cleavedcaspase3 protein, and upregulate the expression of MMP9 and VEGF protein by activating the NFkκB signaling pathway, and it can promote cell proliferation and vascular growth, and protect the neurological function of brain injury rats.