Objective: To investigate whether Treatment with scalp electroacupuncture exerts its effects on attenuating rt-PA-induced blood-brain barrier injury and hemorrhagic transformation after rat acute ischemic stroke by Wnt/?-catenin signaling pathway.Methods: 25 Sprague-Dawley rats were divided into five groups with Random Number Table as follows: Sham group,Vehicle group,rt-PA group rt-PA+IM-12 group,and rt-PA+IM-12 +scalp electroacupuncture(SEA)group,and all SD rats were subjected to a middle cerebral artery occlusion(MCAO)model of ischemic stroke except the rats of Sham group,and then the above groups were respectively administered 1 mL of dimethyl sulfoxide(1 % DMSO in saline),1 ml DMSO,recombinant tPA(rt-PA)(10 mg/kg),rt-PA(10 mg/kg)combined with IM-12(25 mg/kg,dissolved in 1 mL 1 % DMSO),or rt-PA(10 mg/kg)combined with IM-12(25 mg/kg,dissolved in 1 mL 1 % DMSO)and SEA(30minutes)at 4 hours after MCAO.SD rats in each group after treatment were set detections for functional morphology and molecular biology at 24 hours after MCAO as follows: the neurologic deficit score was used to detecte the neurological function of SD rats;the volume of cerebral infarction was evaluated by Tetramethylammonium trichloride staining;the degree of brain edema was measured by standard dry-wet method;blood brain barrier was evaluated by Evans blue extravasation index(EBI);the cerebral hemorrhage was detemined by the content of hemoglobin which was measured by spectrophotometry;the changes of ?-catenin,GSK-3? and tight-junction proteins Occludin,ZO-1,ZO-2 and Claudin-3 were detected by Western Blot analysis.Results: 1.SEA could reduce the neurological defect score and promote the recovery of nerve function in rats after MCAO treated by rt-PA.2.SEA could reduce cerebral infarction volume and cerebral water content of rats after MCAO treated by rt-PA.3.SEA decreased evans blue extravasation index(EBI)and hemoglobin content in MCAO rats after rt-PA treatment.4.SEA decreased the expression of GSK-3? in rats after MCAO treated by rt-PA,and increased the expression of ?-catenin and tight junction proteins when phosphorylated.Conclusions : SEA could attenuate BBB damage via activation of Wnt/?-catenin signaling pathway,thereby reducing the risk of rt-PA-mediated HT and promoting the recovery of neurological function after rats acute ischemic stroke. |