【摘 要】
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Objective:To investigate the effect and potential mechanisms of rutaecarpine (Rut) in a rat artery balloon-injury model.Meods:The intimal hyperplasia model was established by rubbing the endothelia with a balloon catheter in the common carotid artery (CCA
【机 构】
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Key Laboratory of Basic Pharmacology of Guizhou and Department of Pharmacology, Zunyi Medical Colleg
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Objective:To investigate the effect and potential mechanisms of rutaecarpine (Rut) in a rat artery balloon-injury model.Meods:The intimal hyperplasia model was established by rubbing the endothelia with a balloon catheter in the common carotid artery (CCA) of rats.Fifty rats were randomly divided into five groups,ie.sham,model,Rut (25,50 and 75 mg/kg) with 10 rats of each group.The rats were treated with or without Rut (25,50,75 mg/kg) by intragastric administration for 14 consecutive days following injury.The morphological changes of the intima were evaluated by hematoxylin-eosin staining.The expressions of proliferating cell nuclear antigen (PCNA) and smooth muscle (SM) α-actin in the ateries were assayed by immunohistochemical staining.The mRNA expressions of c-myc,extracellular signal-regulated kinase 2 (ERK2),MAPK phosphatase-1 (MKP-1) and endothelial nitric oxide synthase (eNOS) were determined by real-time reverse transcription-polymerase chain reaction.The protein expressions of MKP-1 and phosphorylated ERK2 (p-ERK2) were examined by Western blotting.The plasma contents of nitric oxide (NO) and cyclic guanosine 3\',5\'-monophosphate (cGMP) were also determined.Results:Compared with the model group,Rut treatment significantly decreased intimal thickening and ameliorated endothelial injury (P＜0.05 or P＜0.01).The positive expression rate of PCNA was decreased,while the expression rate of SM α-actin obviously increased in the vascular wall after Rut (50 and 75 mg/kg) administration (P＜0.05 or P＜0.01).Furthermore,the mRNA expressions of c-myc,ERK2.and PCNA were downregulated while the expressions of eNOS and MKP-1 were upregulated (P＜0.05 or P＜0.01).The protein expressions of MKP-1 and the phosphorylation of ERK2 were upregulated and downregulated after Rut (50 and 75 mg/kg) administration (P＜0.05 or P＜0.01),respectively.In addition,Rut dramatically reversed balloon injury-induced decrease of NO and cGMP in the plasma (P＜0.05 or P＜0.01).Conclusion:Rut could inhibit the balloon injury-induced carotid intimal hyperplasia in rats,possibly mediated by promotion of NO production and inhibiting ERK2 signal transduction pathways.
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