摘要
目的 :观察益肺抗纤方抗肺纤维化的作用。方法 :实验用雄性Wistar大鼠分为 4组 ,对照组、模型组、益肺抗纤方组、地塞米松组 ;对照组气管内注入生理盐水 ,其余 3组气管内注入博莱霉素制作大鼠肺纤维化模型。造模后 ,益肺抗纤方组给益肺抗纤方 10ml/kg灌胃 ,地塞米松组给地塞米松 1.5mg/kg腹腔注射 ,模型组和对照组均给生理盐水灌胃 ,均给药 1次 /d。观察各组大鼠肺部病理变化 ,测定各组第 7d、2 8d肺组织超氧化物歧化酶(SOD)、脂质过氧化物 (LPO)和羟脯氨酸 (HP)的含量。结果 :气管内注入博莱霉素第 2 8d时 ,模型组多呈 3级肺纤维化和 1级肺泡炎改变 ;益肺抗纤方组多呈 1级纤维化改变 ,肺泡炎不明显 ;地塞米松组多呈 1级纤维化和 1~ 3级肺泡炎改变 ;对照组呈正常肺结构。第 2 8d时 ,模型组和地塞米松组肺组织SOD活性均较对照组明显下降 (P <0 .0 1和P <0 .0 5 ) ,地塞米松组较模型组SOD活性下降更明显 (P <0 .0 5 ) ;益肺抗纤方组与对照组之间SOD活性无明显差别。对照组、模型组、益肺抗纤方组肺组织LPO含量明显低于地塞米松组 (P <0 .0 1) ;益肺抗纤方组与对照组和模型组之间无明显差别。结论 :益肺抗纤方可通过提高SOD活性 ,降低脂质过氧化 ,减轻氧自由基损伤 ,抑制胶原沉积 。
Aim:To study the effects of Yifeikangxianfang on bleomycin inducing pulmonary fibrosis in rats.Methods:Wistar rats were randomly allocated into 4 groups:the control group,the model group,the yifeikangxianfang therapy group,and the dexomethasone(DXM) therapy group.The normal group was injected with normal saline through trachea,and the other 3 groups were injected with bleomycin to induce experimental pulmonary fibrosis disease model. Yifeikangxianfang group was treated with Yifeikangxianfang 10 ml/kg through gastric,DXM therapy group was injected with DXM 1.5 mg/kg through abdominal cavity,and the other 2 groups were treated with normal saline through gastric.Each group was treated once per day. Pulmonary pathology changes were observed,and the contents of SOD,LPO, and HP were detected at the 7th and 28th day respectively.Results:At the 28th day, the model group's pulmonary pathology changes were on Ⅲ degree pulmonary fibrosis and 1~3 degree alveolitis, and that of the normal group was normal.The level of SOD in the model group and DXM group were decreased than that of normal group,while that of Yifeikangxianfang group had no significant difference compared with normal group.The level of SOD of DXM group was decreased in comparison with the other 3 groups.The contents of LPO in normal group, the model group and yifeikangxianfang group were lower than that of DXM group.Conclusions:It is suggested that yifeikangxianfang could decrease lipid peroxidation,relieve the impairment of oxide radicals,inhibit collagen deposition, and protect pulmonary tissues.
出处
《郑州大学学报(医学版)》
CAS
北大核心
2003年第4期557-560,共4页
Journal of Zhengzhou University(Medical Sciences)