[Effects of acupoint-embedment of medicated-thread and acupoint-injection on expression of cortical urokinase-type plasminogen activator and plasminogen activator inhibitor-1 in rats with cerebral ischemia-reperfusion injury].

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.