RESUMO
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 (Al) group (n=18), and acupoint-thread-embedment (ATE) group (n=18). Rats of the latter 4 groups were randomized into 1 d, 3 d and 5 d 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 Al group, Chuanxiongzine (0.1 mL/200 g) was injected into "Baihui" (GV 20) and "Dazhui" (GV 14), 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 GV 20 and GV 14, 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 Al 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.