RESUMEN
Objective To explore the effect of celecoxib on neural function in rats with acute intracerebral hemorrhage.Methods SD rats were randomly divided into sham group,model group,inhibitor group and celecoxib group.Except the sham operation group,the cerebral hemorrhage model was made by autologous blood injection in each group.Rats in the inhibitor group were injected with extra cellular regulated protein kinase(ERK)inhibitor(DCZ19931)into the anterior ventricle on the basis of the model group.Celecoxib group rats were injected intraperitoneally with 100 mg·kg 1·d-1 celecoxib,for 2 weeks.The degree of neurological injury in rats was compared by Longa five-grade score.The water content of brain tissue of rats in each group was detected and the expression of aquaporin 4(AQP4)in brain tissue of rats in each group was detected by Western blotting.Enzyme-linked immunosorbent assay was used to detect the content of interleukin-1(IL-1β),tumor necrosis factor-α(TNF-α),superoxide dismutase(SOD)and malonaldehyde(MDA)in the brain tissue of rats in each group.Western blotting was used to detect the expression of mitogen-activated protein kinase(MAPK)/ERK signal pathway protein in rats of each group.Result Compared with sham group,the neurological function score,brain water content,relative expression level of AQP4 protein,content of IL-1β,TNF-α and MDA,relative expression levels of p-ERK1 protein,p-ERK2 protein and MAPK protein in model group were significantly increased,while content of SOD was significantly decreased(P＜0.05).Compared with model group,the neurological function score,brain water content,relative expression level of AQP4 protein,content of IL-1β,TNF-α and MDA,relative expression levels of p-ERK1 protein,p-ERK2 protein and MAPK protein in inhibitor group and celecoxib group were significantly decreased,while content of SOD was significantly increased(P＜0.05).Conclusion Celecoxib can effectively improve the neurological function of rats with acute intracerebral hemorrhage,and its mechanism may be related to the regulation of MAPK/ERK signal pathway and inhibition of inflammation.