OBJECTIVE: To observe the effect of electroacupuncture (EA) intervention on expression of Slit 2 and its transmembrane receptor Robo 1 in the cortex tissue of cerebral infarction rats so as to study its mechanism underlying improvement of cerebral ischemia. METHODS: Ninety male Sprague Dawley rats were randomly divided into control group (n = 10), model group (n = 40) and EA group (n = 40), and the latter two groups were further randomized into four subgroups: 1 d, 3 d, 7 d, and 14 d (n = 10 in each subgroup) according to the cerebral ischemia duration. Cerebral infarction model was established by occlusion of the middle cerebral artery (MCAO). EA (80-100 Hz, 1-3 mA) was applied to bilateral "Neiguan" (PC 6) and "Zusanli" (ST 36) for 30 min, once daily for 1 d, 3 d, 7 d, and 14 d, respectively. The animals' neurological defect was assessed using Zea-Longa scoring. The expression of Slit 2 and Robo 1 proteins in the cerebral cortex on the ischemic side was assayed using immunohistochemistry and Western blotting, respectively. RESULTS: In comparison with the control group, the neurological score was significantly higher in the model group (P < 0.05), and reduced considerably on day 7 and 14 after MCAO in the EA group compared with the model group (P < 0.05). Immunohistochemical results showed that in comparison with the control group, the immunoactivity levels of cerebral Slit 2 and Robo 1 were remarkably upregulated on day 1, 3 and 7 after MCAO in the model group (P < 0.05, P < 0.01), and backed to the control levels on day 14 (P > 0.05). While compared with the model group, the immunoactivity levels of cerebral Slit 2 and Robo 1 were further obviously upregulated on day 1, 3, 7 and 14 after cerebral ischemia in the EA group (P < 0.05, P < 0.01). The results of Western blotting about the expression levels of cerebral Slit 2 and Robo 1 proteins were nearly the same to those of immunohistochemical outcomes in the 4 subgroups apart from that the expression levels of both Slit 2 and Robo 1 proteins were still obviously higher on day 14 after MCAO in the model group (P < 0.01). CONCLUSION: EA intervention can significantly improve cerebral ischemia rats' neurological function and obviously upregulate the expression of cerebral Slit 2 and Robo 1 proteins, which may be one of the mechanisms of EA therapy for relieving cerebral infarction in clinic.
OBJECTIVE: To observe the effect of electroacupuncture (EA) intervention on expression of Slit 2 and its transmembrane receptor Robo 1 in the cortex tissue of cerebral infarctionrats so as to study its mechanism underlying improvement of cerebral ischemia. METHODS: Ninety male Sprague Dawley rats were randomly divided into control group (n = 10), model group (n = 40) and EA group (n = 40), and the latter two groups were further randomized into four subgroups: 1 d, 3 d, 7 d, and 14 d (n = 10 in each subgroup) according to the cerebral ischemia duration. Cerebral infarction model was established by occlusion of the middle cerebral artery (MCAO). EA (80-100 Hz, 1-3 mA) was applied to bilateral "Neiguan" (PC 6) and "Zusanli" (ST 36) for 30 min, once daily for 1 d, 3 d, 7 d, and 14 d, respectively. The animals' neurological defect was assessed using Zea-Longa scoring. The expression of Slit 2 and Robo 1 proteins in the cerebral cortex on the ischemic side was assayed using immunohistochemistry and Western blotting, respectively. RESULTS: In comparison with the control group, the neurological score was significantly higher in the model group (P < 0.05), and reduced considerably on day 7 and 14 after MCAO in the EA group compared with the model group (P < 0.05). Immunohistochemical results showed that in comparison with the control group, the immunoactivity levels of cerebral Slit 2 and Robo 1 were remarkably upregulated on day 1, 3 and 7 after MCAO in the model group (P < 0.05, P < 0.01), and backed to the control levels on day 14 (P > 0.05). While compared with the model group, the immunoactivity levels of cerebral Slit 2 and Robo 1 were further obviously upregulated on day 1, 3, 7 and 14 after cerebral ischemia in the EA group (P < 0.05, P < 0.01). The results of Western blotting about the expression levels of cerebral Slit 2 and Robo 1 proteins were nearly the same to those of immunohistochemical outcomes in the 4 subgroups apart from that the expression levels of both Slit 2 and Robo 1 proteins were still obviously higher on day 14 after MCAO in the model group (P < 0.01). CONCLUSION: EA intervention can significantly improve cerebral ischemiarats' neurological function and obviously upregulate the expression of cerebral Slit 2 and Robo 1 proteins, which may be one of the mechanisms of EA therapy for relieving cerebral infarction in clinic.