Effect Of Electro-acupuncture On Expression Of Netrin-1and Semaphorin3a In Rat Cortex After Middle Cerebral Occlusion

Objective To observe the expression of netrin-1(Ntn1) andsemaphorin-3a (sema3a) in the cortex of rats after middle cerebralocclusion (MCAO)，and determine the effect of electro-acupuncture (EA)intervention on their expression，so as to explore the roles of Ntn1andsema3a in neural plasticity after cerebral infarction．Methods A total of135male Sprague Dawley (SD) rats were randomlydivided into control group (n=15)，model group (n=60) and EA group(n=60，in the acupuncture points PC6and ST36，80to100Hz，1to3mA，1to3V，for30min，performed in90min after anesthesia recovery)，and further assigned into4time point，that is，in1d，3d，7d and14d aftermodel establishment． Modified modified neurologic severity scores(mNSS) were carried out to evaluate neurologic injury at every timepoint． Immunohistochemical assay was used to detect the expression anddistribution of Ntn1， sema3a and NF200in the cortical ischemicregion．Western blotting was employed to detect the expression of Ntn1andsema3a in the affected cortex． Results Immunohistochemical results showed that the rat brain cortexexpressed Ntn1and sema3a at every time point，and they mainly located inthe cytoplasm．Western blotting indicated that the model group had higherexpression of Ntn1at1d (P＜0.01)，kept in elevation at3d (P＜0.01)，reached peak at7d (P＜0.01)，and maintained still higher at at14d than normal levels (P＜0.01).Compared with the control group，theexpression of Ntn1in EA group had the same trend，but the expressionlevel was significantly higher than the model group,with significantdifferences in1d，3d，7d and14d (P＜0.05，P＜0.01)． Compared withthe control group，sema3a protein level in the model group began to rise in1d after model surgery (P＜0.01)，increased and reached the peak in7d(P＜0.01)，and was still higher than the normal level in14d (P＜0.01)．Compared to the model group，EA group presented low expression ofsema3a at the same time point，with significant differences in1d，3d，7dand14d (P＜0.05，P＜0.01)，and reached peak in7d． The results ofWestern blotting and immunohistochemical assays were basicallyconsistent．Compared with model group，the mNSS of EA group hadsignificant differences in7and14d (P＜0.05)． Significant differencewas seen in the expression of NF200between model group and EA groupin14d (P＜0.05)．Conclusion Cerebral infarction significantly up-regulates the expressionof Ntn1and sema3a.EA intervention improves Ntn1expression but suppresses sema3a,and promotes axon regeneration and repair，which maybe one of the mechanisms that EA promotes the recovery of neurologicalfunction after cerebral infarction．...