Abstract: Objective To detect expressive changes of MKP-1 and measure NO content in the rats of pericontusional cerebral cortex after traumatic brain injury (TBI), discuss regulatory role and molecular mechanism of MKP-1 on NO generation after TBI. Methods We constructed TBI model by the Feeney's method. Nitric oxide detection kits were used to measure NO content in pericontusional cerebral cortex between control group and TBI group. Distribution of MKP-1 was detected by immunohistochemistry. Western blot analysis were performed to detect expression level of MKP-1, endothelial NOS and MAPKs in the rats of pericontusional cerebral cortex after TBI. Result NO level significantly decreased at 3h、6h、24h and 72h with concentration as 20.8 ± 2.5 μmol/L 、23.9 ± 3.8 μmol/L 、24.0 ± 1.6 μmol/L 、26.8 ± 2.6 μmol/L (P<0.05) respectively, compared with the control as 34.4 ± 3.2 μmol/L after TBI. The positive staining MKP-1 cells were scattered distributed in pericontusional cerebral cortex with brown cytoplasma and processes and increased significantly at 3h and 6h after TBI. Compared to the control group, the protein expressions of MKP-1 were increased at 3h and 6h respectively with normal level at 24h after TBI(P<0.05). While the protein levels of eNOS were decreased at 3h and 6h respectively after TBI (P<0.05). The protein expressions of pERK and p-p38 were both decreased at 3h and 6h respectively after TBI compared with control group (P<0.05).Conclusion Increased MKP-1 expression in pericontusional cerebral cortex after TBI specifically decreased the expression level of pERK and p-p38 MAPK with the pJNK intact to down-regulated the expression of endothelial NOS, which decreased NO content attributed to the defect of cerebral blood flow.

Key words: Key words：rats, traumatic brain injury, MKP-1, NO