摘要
目的:探讨贝母合剂对博来霉素肺损伤大鼠血管内皮功能的干预作用。方法:40只大鼠随机分为4组:假手术组、模型组、地塞米松组和贝母合剂组,后3组建立博来霉素肺损伤模型,地塞米松组和贝母合剂组分别予地塞米松、贝母合剂治疗。用免疫组化SP法检测肺组织AQP1、ICAM-1和VCAM-1,并采用光学显微镜和Image Pro Plus6.0测量计算其平均光密度(IOD)值。结果:模型组大鼠肺组织AQP1表达显著低于假手术组(P<0.01),而ICAM-1、VCAM-1表达显著高于假手术组(P<0.01)。与模型组相比,贝母合剂组肺组织AQP1表达明显升高(P<0.01),ICAM-1、VCAM-1表达明显降低(P<0.01);地塞米松组肺组织ICAM-1、VCAM-1表达低于模型组(P<0.01,P<0.05),而AQP1表达与模型组无显著性差异(P<0.05)。结论:促进肺损伤大鼠肺组织AQP1表达和抑制ICAM-1、VCAM-1表达可能是贝母合剂防治肺损伤的作用机制之一。
Objective:To investigate the intervention effect of Fritillaria Mixture on endothelial function in rats with PYM-induced lung injury.Methods:40 rats were randomly divided into sham operation group,model group,dexamethasone group and Fritillaria Mixture group and then injected BLM 5 mg / kg by intratracheal way to copy lung injury model.Dexamethasone group was treated with dexamethasone distilled in water and Fritillaria Mixture group was treated with Fritillaria Mixture.The expressions of AQP1,ICAM-1 and VCAM-1 in lung tissue were tested by immunohistochemistry SP method.The average optical density(IOD) of AQP1,ICAM-1 and VCAM-1 were calculated by optical microscopy and Image Pro Plus6.0.Results:The degree of AQP1 in lung tissue of model group rats was significantly lower than that of sham operated group rats(P〈0.01) but the degree of ICAM-1 and VCAM-1 was significantly higher(P〈0.01).Compared with model group,the degree of AQP1 in lung tissue of Fritillaria Mixture group was significantly higher(P〈0.01) and the degree of ICAM-1 and VCAM-1 was significantly lower(P〈0.01).The degree of ICAM-1 and VCAM-1 in lung tissue was lower than that of model group rats(P〈0.01,P〈0.05) while the degree of AQP1 showed no difference(P〈0.05).Conclusion:To stimulate the expression of AQP1 and inhibit the expression of ICAM-1 and VCAM-1 in lung tissue of rats with BLM-induced lung injury is probably one of the mechanisms that Fritillaria Mixture treats BLM-induced lung injury.
出处
《辽宁中医杂志》
CAS
北大核心
2015年第2期423-425,共3页
Liaoning Journal of Traditional Chinese Medicine
基金
国家自然科学基金资助项目(81373603)