CVA模型大鼠痰瘀同治气道炎症TGF-β1、IL-13、VEGF及NF-κB之间的相关性研究  

Correlative Study Between Airway Inflammation and Serum TGF-β1,IL-13,VEGF,NF-κB in Rats with CVA by Phlegm and Blood Stasis Stagnation

作　　者：李冬梅[1] 施雷[2] 王文丽[1] LI Dong - mei SHI Lei WANG Wen - li(The Affiliated Hospital of Liaoning University of TCM, Shenyang 110032, China TCM Hospital of Huanggu District ,Shenyang 110032, China)

机构地区：[1]辽宁中医药大学附属医院儿科,辽宁沈阳110032 [2]沈阳市皇姑区中医院,辽宁沈阳110032

出　　处：《中医药学报》2016年第6期37-41,共5页Acta Chinese Medicine and Pharmacology

基　　金：沈阳市科技创新专项资金-人口与健康科技公关专项(F14-158-9-09)

摘　　要：目的:探讨痰瘀同治CVA模型大鼠气道炎症及其与TGF-β1、IL-13、VEGF及NF-κB之间的相关性,为从痰瘀论治小儿CVA提供理论支持。方法:雌性SPF级大鼠72只随机分为正常对照组、模型组、辅舒酮组、健脾化痰组、行气化瘀组、痰瘀同治组,每组12只。造模30天后,正常对照组、模型组每天给予生理盐水灌胃,各治疗组给予相应药物灌胃,干预30后取材,观察各组大鼠气道炎症情况并测定血清中TGF-β1、IL-13、VEGF及NF-κB水平。结果:正常对照组大鼠无明显炎症细胞浸润,模型组大鼠支气管周围炎症细胞浸润明显,以嗜酸性粒细胞和淋巴细胞浸润为主,浸润程度明显高于正常对照组(P<0.05);药物干预后大鼠肺组织炎症细胞浸润程度明显减轻,且以痰瘀同治组更明显(P<0.05)。大鼠血清中TGF-β1、IL-13、VEGF及NF-κB的表达水平,模型组显著高于正常对照组(P<0.05);药物干预可抑制TGF-β1、IL-13、VEGF及NF-κB的表达,且痰瘀同治组改善效果更明显(P<0.05)。嗜酸性粒细胞浸润与TGF-β1、IL-13、VEGF及NF-κB表达呈正相关关系(P<0.05)。结论:TGF-β1、IL-13、VEGF及NF-κB在CVA大鼠过度表达,这些因子与CVA气道炎症有很好相关性,痰瘀同治法可抑制这些因子活性,从而减轻和控制CVA气道炎症的作用。Objective： To investigate the phlegm and blood stasis pathogenesis on airway inflammation in cough variant asthma（CVA） model rats and the correlation between airway inflammation and transforming growth factor- β1 （TGF- β1 ）, interleukin - 13 （ IL - 13 ）, vascular endothelial growth factor（ VEGF）, nuclear factor kappa - B （ NF - κB ）, provide theoretical support for the treatment of children with CVA. Methods ： 72 female SPF rats were randomly divided into a normal control group, a model group, a Flixotide group, a phlegm - reducing group, a blood - stasis dispersing group, a phlegm and blood stasis stagnation treatment group, with 12 in each group. Building models after 30 days, and normal control group and model group was lavaged by saline every day, each treatment group were given drug lavage, materials after intervention for 30 days. Observe airway inflammation of rats in each group and the level of serum TGF - β1, IL - 13, VEGF and NF - κB. Results： The rats in normal control group had no obvious inflammatory cell infiltration. Inflammation cell infiltration was significant around bronchial of rats in the model group, mainly eosinophils and lymphocyte. Infiltration degree was significantly higher than that in normal control group （P 〈 0.05 ） ; inflammation cells infiltration reduced significantly in rats＇ lung tissue after drug intervention, and the phlegm and blood stasis stagnation treatment group was more obvious （ P 〈 0. 05 ）. The expressions of TGF - β1, IL - 13, VEGF and NF - κB were significantly higher than those of normal control group （P 〈 0. 05 ） ;the drug intervention could inhibit the expressions of TGF - β1, IL - 13, VEGF and NF - κB, and the effect was more obvious in phlegm and blood stasis stagnation treatment group （P 〈 0.05 ）. Eosinophils infiltration was positively related to TGFβ1, IL - 13, VEGF and NF - κB （P 〈 0.05 ）. Conclusion： The expressions of TGF - β1, IL - 13, VEGF and NF - κB are excessive in CVA rats. Thes

关 键 词：痰瘀同治 咳嗽变异性哮喘模型 气道炎症 转化生长因子-β1 白介素-13 血管内皮生长因子 转录因子蛋白 相关性 

分 类 号：R285.5[医药卫生—中药学]