Objective To observe the effect of acupoint-embedement of medicated-thread and acupoint-injection of Chuanxiongzine on the expression of urokinase-type plasminogen activator(uPA) and plasminogen activator inhibitor-1(PAI-1) in the cerebral cortex in rats with cerebral ischemia-reperfusion injury(CI/RI)

so as to explore its underlying mechanism in protecting the ischemic cerebral tissue.Methods Seventy-eight SD rats were randomly divided into normal control group(n=6)

sham operation(sham) group(n=18)

model group(n=18)

acupoint injection(AI) group(n=18)

and acupoint-thread-embedment(ATE) group(n=18).Rats of the latter 4 groups were randomized into 1d

3d and 5d subgroups

with 6 rats in each.CI/RI model was established by occlusion of the right middle cerebral artery(MCAO) for 30 min and reperfusion.For rats of the AI group

Chuanxiongzine(0.1mL/200g) was injected into "Baihui"(GV20) and "Dazhui"(GV14)

and for those of ATE group

a piece of medicated thread containing collagen protein(extracted from the rat's tail tissue) and Chuanxiongzine + retarder was embedded into GV20 and GV14

respectively.The expression of uPA and PAI-1 in the cerebral cortex on the ischemia side was detected by immunohistochemistry.Results In comparison with the normal control group

the expression of uPA of the ischemia cerebral cortex on day 1

3 and day 5 in the model group was increased significantly(P<0.01)

while the PAI-1 expression decreased remarkably in the model group(P<0.01).Compared with the 3 time-points of the model group

cortical uPA expression levels at the 3 time-points in the AI group and those of day 3 and day 5 in the ATE group were down-regulated significantly(P<0.01)

whereas cortical PAI-1 expression levels at the 3 time-points in both AI and ATE groups up-regulated considerably(P<0.05

P<0.01).Comparison between AI and ATE groups showed that the expression levels of cortical uPA in the latter group on day 3 and day 5 were significantly lower than those of the former group(P<0.05)

whereas the cortical PAI-1 expression levels in the latter group on day 3 and day 5 were evidently higher than those of the former group(P<0.05).But

cortical PAI-1 expression of the ATE group on day 1 was significantly lower than that of the AI group(P<0.05).No significant differences were found between the AI and ATE groups in the expression level of cortical uPA on day 1 and between normal and sham groups in both uPA and PAI-1 expression levels at the 3 time-points(P>0.05).Conclusion Both AI and ATE can down-regulate cortical uPA expression and up-regulate cortical PAI-1 expression in rats with CI/RI

which may contribute to their protective effect in reducing cerebral ischemic injury.