复方甘草甜素对博莱霉素致肺纤维化大鼠的实验研究

目的:观察复方甘草甜素对博莱霉素致肺纤维化模型大鼠肺组织匀浆中超氧化物歧化酶SOD的活性及丙二醛MDA含量的影响,探讨复方甘草甜素在大鼠肺纤维化中的作用机理。方法:126只清洁级SD雄性大鼠,随机分成正常对照组(A组)、博来霉素模型组(B组)、地塞米松干预组(C组)、复方甘草甜素大、中、小剂量组(D、E、F组),每组各21只,除A组外,其余各组采用博莱霉素复制大鼠肺纤维化模型,造模第2天起,D、E、F组每天分别腹腔内注射复方甘草甜素,C组用地塞米松腹腔内注射,A、B组用生理盐水腹腔内,每组分别于7、14、28天随机处死7只大鼠,采集肺组织,制作匀浆,检测各组肺组织匀浆中SOD的活性及MDA含量的变化。结果:复方甘草甜素能提高肺组织匀浆中的SOD活性,降低MDA的含量。结论:复方甘草甜素对肺纤维化大鼠的作用机制,可能与通过调节其体内自由基水平,减轻自由基对肺组织结构的氧化损伤有关,而且复方甘草甜素大剂量组的作用优于中小剂量组,呈一定的量效关系。

Experimental Study on Effect of Stronger NEO-Minophagen C in Treating Rats with Bleomycin-induced Pulmonary Fibrosis

Objective: To observe the influence of Stronger NEO-Minophagen C(SNMC) on the level of SOD and MDA from the lung tissues in rats with bleomycin-induced pulmonary fibrosis.Methods:126 healthy SD rats,were randomly divided into 6 groups(n= 21,each):normal control group(group A),bleomycin model group(group B),Dxm group(group C),SNMC of high group(group D),SNMC of moderate and low dosage(group D,E,F).The rat model was induced by bleomycin and respective medicine was given to each group.Every group was sub-divided into three groups(n=7) which was killed in the 7th,14th and 28th day.Then,to check the level of SOD and MDA from the lung tissues in the rats.Results : SNMC could increase the activity of SOD,and lower the contents of MDA from the lung tissues in the rats.Conclusion: SNMC can decrease harmful free radical and increase beneficial free radical scavenger in lung tissue,lesson the oxidative injury of pulmonary tissues caused by free radical in pulmonary fibrosis rats.That is probably the mechanism of SNMC protecting pulmonary tissues.In the same time,it has dose-effect relationship in the change above.