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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 Bimu mixture on endothelial function of bleomycin-induced lung injury in rats. Methods: Forty rats were randomly divided into 4 groups: sham-operation group, model group, dexamethasone group and bommellix group. The latter 3 groups were established bleomycin-induced lung injury model, dexamethasone group Respectively dexamethasone, Fritillaria mixture treatment. The lung tissues AQP1, ICAM-1 and VCAM-1 were detected by immunohistochemical SP method, and the average optical density (IOD) value was calculated by optical microscope and Image Pro Plus 6.0. Results: The expression of AQP1 in model group was significantly lower than that in sham operation group (P <0.01), while the expression of ICAM-1 and VCAM-1 in model group was significantly higher than that in sham operation group (P <0.01). Compared with the model group, the expression of AQP1 in the lung tissue of the BMC group was significantly increased (P <0.01) and the expression of ICAM-1 and VCAM-1 was significantly decreased (P <0.01) -1 expression was lower than the model group (P <0.01, P <0.05), while the AQP1 expression was not significantly different from the model group (P <0.05). CONCLUSION: AQP1 expression and ICAM-1, VCAM-1 expression in the lung tissue of rats with lung injury may be one of the mechanisms of Fumuli Mixture in preventing and treating lung injury.