| Ischemic cerebrovascular disease is a kind of common and frequently-occurring disease in clinic. Because of higher morbidity, mortality and disability, it brings tremendous mental stress and economic burden to individuals, families and society. As a traditional therapy, acupuncture treat the cerebral ischemia have thousands of years in China. Modern electroacupuncture (EA) is gradually developed on the basis of acupuncture, with many the unique advantages:the objective, stable amount of stimulation, the patient tolerated and so on. Electroacupuncture is wildly used in clinic, it can improve neurological deficit scores in the treatment of stroke. Electroacupuncture can reduce focal cerebral ischemia/reperfusion during ischemic neuron dying, up-regulate the brain vascular endothelial growth factor protein, promote angiogenesis and inhibit the inflammatory reaction in ischemia and reperfusion area to protect our brain. Electroacupuncture, which from the surface points, stimulating the endogenous protection mechanism of the body is an effective non-drug treatment way of cerebral ischemia. Studies have found, angiogenesis and endothelial progenitor cells were closely related after cerebral ischemia. There is few studies about mechanism of how the EA to promote EPCs mobilization, migration and homing. Our study is committed to research the effect of EA to the number of EPCs and CXCR4+cells in peripheral blood and EPCs in marrow, the protein content of SDF-1α in peripheral blood of focal cerebral ischemia/reperfusion SD (Sprague-Dawley) rats. Our study explore the effect of EA on EPCs and SDF-1α after focal cerebral ischemia/reperfusion injury. In the perspective of SDF-1/CXCR4axis, our study explore the impact of EA on EPCs migration.Objective1. To investigate the effect of electroacupuncture on the abilities of learning and memory in rat after focal cerebral ischemia/reperfusion.2. To investigate the effect of electroacupuncture and AMD3100on the count of CXCR4+cells in peripheral blood, EPCs in peripheral blood and in marrow of focal cerebral ischemia/reperfusion SD rats.3. To investigate the effect of electroacupuncture on the protein level of SDF-1α in peripheral blood. 4. To investigate the mechanism of electroacupuncture in vasculoge-nesis for focal cerebral ischemia/reperfusion.MethodsThe96male SD rats received filament occlusion of the right middle cerebral artery for2hours. Rats were randomly divided into group A and B, then group A were randomly divided into normal group, model group and EA group, group B were randomly divided into normal group, model group, EA group and drug group. EA was given at the bilateral "Hegu" point (LI4) for15min in the EA group and AMD3100was injected at1.25mg/Kg once in drug group after reperfusion1h. Each group had six rats in group A, the model and EA groups were taken morris water maze test in the third day after reperfusion, detected their the abilities of learning and memory. In gourp B, the model and EA groups were each respectively divided into four subgroups receiving repedusion1,2,3and7days after ischemia, every subgroup have6cases. In every subgroup except drug gourp, Flow cytometer was used to detect EPCs and CXCR4+cells in peripheral blood and EPCs in marrow. SDF-1α protein levels in serum was detected by enzyme linked immunosorbent assay (ELISA). In durg gourp, it was used to detect EPCs and CXCR4+cells in peripheral blood by Flow cytomete. Neurological symptom score was used to evaluate the neurological function impairment of focal cerebral ischemia/reperfusion.Results 1. Neurological symptom scoreNeurological function deficit had been found in all groups and EA can effectively improve the neurological function deficit. At the time points of reperfusion2h, Id,3d, score gradually reduced but the difference between model and EA groups was not statistically significant (P>0.05). With prolonged reperfusion, the rats have a recovery of neurological function, at the time points of7d the difference between model and EA groups was significantly different (P<0.05)2. Morris water maze test(1) Place navigation testThe escape latency period:The escape latency period were shortened with the increase of the number of training in each gourps. In Morris water maze test, normal and model group compared with EA gourp respectively were not statistically significant (P>0.05) at Id, no significant difference between EA and normal group (P>0.05) at2d. EA and model group compared with normal gourp respectively were significantly different (P<0.05) at3d. EA group compared with normal and model gourp respectively were significantly different (P<0.05) at4d, but no significant difference of the escape latency period between EA and Normal group at5d.(2) Spatial probe testThe time spending in the former platform quadrant:in sixth day the platform removed, the time of EA and normal group spent in the former platform quadrant was significantly longer than model group (P<0.05)The frequency of crossing former platform sit:significantly increased the frequency of crossing former platform sit in EA and normal group, which compared with model group were significantly different (P<0.05) There is no significant difference between EA and normal group.3. Test of detected EPCs and CXCR4+cells in peripheral blood, EPCs in marrow and SDF-1α in serum(1) The change of EPCs counts in peripheral bloodCompared with the corresponding normal group, focal cerebral ischemia/reperfusion rats counts of EPCs in blood at Id in model and EA group both increased significantly (P<0.01), The EPCs counts in EA groups was higher than the model group (P<0.05) at2d. At3d and7d the count of EPCs in peripheral blood was slightly higher than the normal group in EA and model group (P>0.05). Each Point in time the count of EPCs of normal and drug group was no significant difference in peripheral blood (P>0.05)(2) The change of CXCR4+cell counts in peripheral bloodCompared with the corresponding normal group, focal cerebral ischemia/reperfusion rats counts of CXCR4+cell in blood at Id in model and EA group both increased significantly (P<0.01), EA group increased to a maximum and was significantly higher than model groups (P<0.01)at2d. EA group was still significantly higher than other groups (P<0.05) at3d. model and EA group compare with normal gourp respectively were significantly different (P<0.05) at7d. At each time points, the count of CXCR4+cells of normal and drug group was no significant difference in peripheral blood (P>0.05)(3) The change of SDF-1α levels in serumModel group and EA group serum SDF-1α protein levels increased to a maximum, and statistically significant compared with the normal group (P<0.05, P<0.01) at Id. Model and EA group in serum of SDF-1α protein level were lower those of Id, EA group compared with normal group difference still was significant (P<0.01) at2d. Serum of SDF-1α protein level differences between model and EA group was not statistically significant (P>0.05), but both were higher than normal group, had a statistically significant difference (P<0.05) at3d. In each group between serum of the SDF-1α protein level was no significant difference (P>0.05).(4) The change of EPCs counts in marrowEPCs counts of Model group increased to a maximum, compared with the normal group was significantly higher (P<0.01) at Id. The EA group bone marrow the count of EPCs was significantly higher than the normal and model group (P<0.05, P<0.01) at2d. EA compare with normal group was statistically significant (P<0.01) at3d. In each group between bone marrow the count of EPCs was no significant difference (P>0.05) at7d. Conclusions1. EA can promote recovery of neurological function after focal cerebral ischemia/reperfusion.2. EA can improve the learning and memory abilities after focal cerebral ischemia/reperfusion.3. EA can increase the count of EPCs and CXCR4+cell.4. EA can increase the count of EPCs in marrow5. EA can increase the expression of SDF-1α protein in peripheral blood increased.6. EA can increase the count of EPCs in peripheral blood and marrow of focal cerebral ischemia/reperfusion injury rats, which may contribute to its effect of upregulating SDF-1α. |
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