| 摘要: |
| 目的 观察局灶性脑梗死大鼠皮质Slit2、SrGAP1的表达和电针对其表达的影响;探讨电针对脑梗死后神经可塑性的作用机制。 方法 将60只雄性SD大鼠随机分为模型组(n=30)和电针组(n=30),根据电针治疗时间分为0 d(n=10)、7 d(n=10)、14 d(n=10)三个亚组。用线栓法栓塞模型组、电针组大鼠大脑中动脉1.5 h后恢复血流。在0、7、14 d时用尼氏染色观察大脑梗死灶周围组织形态学变化;用免疫荧光、蛋白质印迹法检测缺血侧大脑皮质Slit2和SrGAP1的表达。 结果 神经功能评分(mNSS)结果表明,0 d 时模型组与电针组相比差异无统计学意义(P>0.05),7、14 d时电针组的神经功能评分低于模型组(P<0.01)。尼氏染色表明,0 d时电针组与模型组相比无差异,均有尼氏体数量少、排列紊乱、伴有大脑水肿;7 d时与模型组相比,电针组尼氏体增多,但排列紊乱;14 d时与模型组相比,电针组尼氏体增多,排列整齐。免疫荧光、蛋白质印迹表明,0 d时电针组与模型组相比大鼠Slit2、SrGAP1荧光强度及灰度值差异无统计学意义(P>0.05), 7、14 d时电针组荧光强度及灰度值高于模型组(P<0.05),0 d模型组低于7 d模型组(P<0.05),7 d模型组高于14 d模型组(P<0.05),0 d电针组低于7 d电针组(P<0.05),7 d电针组高于14 d电针组(P<0.05)。 结论 局灶性脑梗死后,0 d组大鼠Slit2、SrGAP1低表达,电针治疗7、14 d后可促进Slit2、SrGAP1表达并延长其高表达时间,促进轴突的再生和修复,这可能是电针促进脑梗死后神经功能恢复的机制之一。 |
| 关键词: 脑缺血 再灌注损伤 电针 Slit2 SrGAP1 |
| DOI：10.16781/j.0258-879x.2016.01.0046 |
| 投稿时间：2015-05-19修订日期：2015-07-03 |
| 基金项目:重庆市科委自然科学基金(CSTC, 2010BB5380; cstc2014jcyiA10043), 重庆市教教育委员会科学技术研究项目(KJ130323). |
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| Effect of electro-acupuncture on expression of Slit2 and SrGAP1 in rats with focal cerebral infarction |
| LONG Fei,LI Xue-zhi*,GONG Biao,WANG Ying,DAI En-ze,GUO Quan-hu |
(Department of Acupuncture and Massage, Traditional Chinese Medicine College, Chongqing Medical University, Chongqing 400016, China
*Corresponding author.) |
| Abstract: |
| Objective To observe the effect of electro-acupuncture (EA) intervention on expression of Slit2 and SrGAP1 in rats with focal cerebral infarction and to study the underlying mechanism of EA intervention on neuronal plasticity after cerebral ischemia. Methods Sixty male Sprague Dawley rats were randomly divided into Model group(n=30) and EA group (n=30); and according to elctro-apunture treatment duration, both 2 groups were further randomized into 3 subgroups:0 d(n=10),7 d(n=10), and 14 d (n=10).The middle cerebral arteries of the model group and EA group were embolized for 1.5 hours by suture. Nissl staining, immunofluorescence method and Western blotting analysis were sued to observe the histology and morphology change around the cerebral infarction and to assay the expression of Slit2 and SrGAP1 in the cerebral cortex on the ischemic side on day 0, 7, and 14. Results In comparison with the model group, the neurological score of EA group had no obvious difference on day 0 (P>0.05) and was significantly lower on day 7 and day 14 (P<0.01). Nissl staining results showed that in comparison with the model group, EA group had no obvious difference and both groups had reduced nissl body number, disordered array and brain edema on day 0; even on day 7 the nissl bodies were still disordered in the EA group, but the nissl body number increased obviously; while on day 14 the EA group had increased and well arrayed nissl bodies. Immunofluorescence method and Western blotting analysis showed that the fluorescence intensities and grey levels of rat Slit2 and SrGAP1 had no significant differences between model group and EA group on day 1(P>0.05); but on day 7 and day 14, the fluorescence intensities and grey levels of EA group were significantly higher than those of the model group(P<0.05). In the model group the above values on day 0 were significantly lower than those on day 7 (P<0.05), and those on day 7 were significantly higher than those on day 14 (P<0.05). In the EA group the fluorescence intensities and grey levels on day 0 were significantly lower than those on day 7 (P<0.05), and those on day 7 were significantly higher than those on day 14 (P<0.05). Conclusion Slit2 and SrGAp1 are lowly expressed following focal cerebral infarction on day 0, and EA intervention for one and two weeks can promote their expression and prolong the duration of high expression, subsequently accelerating axonal regeneration and repair, which may be a mechanism of EA therapy for neurological function recovery following cerebral infarction. |
| Key words: brain ischemia reperfusion injuries electroacupuncture Slit2 SrGAP1 |
