黄芩苷对肺纤维化大鼠肺组织氧化应激的反应及炎症细胞的影响  

Impact of Baicalin on Oxidative Stress and Inflammatory Cell in Pulmonary Fibrosis

作　　者：王清华[1] 姚旭[1] 魏新智[1] 闵冬雨[1] 任延毅 庞立健[2] 吕晓东[2] 

机构地区：[1]辽宁中医药大学附属医院,辽宁沈阳110032 [2]辽宁中医药大学,辽宁沈阳110847

出　　处：《中华中医药学刊》2017年第6期1382-1384,I0007,I0008,共5页Chinese Archives of Traditional Chinese Medicine

基　　金：国家自然科学基金面上项目(81373579)

摘　　要：目的:研究黄芩苷对特发性肺纤维化炎症细胞的影响及在氧化应激时的作用。方法:采用博来霉素复制特发性大鼠肺纤维化模型,给予黄芩苷干预后,ELISA法检测肺组织中TNF-α和IL-1β、MDA含量和SOD活力;吉姆萨染色检测支气管肺泡灌洗液中炎症细胞的计数。结果:黄芩苷能降低肺组织中TNF-α和IL-1β,降低MDA的含量,增加SOD的活性;支气管肺泡灌洗液中炎症细胞显着降低。结论:黄芩苷可能通过抑制炎症反应及增加细胞抗氧化能力来抑制肺纤维化。Objective： To observe the effect of baicalin on inflammatory cell and the oxidative stress in lung tissue of rat pulmonary fibrosis. Methods： Pulmonary fibrosis model was constituted by injecting bleomycin in tracheas of rats which were treated with baicalin injected in cavum-abdominis. Kill animals on the 28 th day. Determine concentrations of TNF-α,IL-1β,MDA and SOD in lung tissue by enzyme-linked immunosorbent assay and inflammatory cell counts in bronchoalveolar lavage fluid by Wright-Giemsa. Results： The expressions of TNF-α and IL-1β in lung tissue of baicalin group were significantly lower than that of model groups（ P〈0. 01）. The content of MDA was lower and the activity of SOD of baicalin group was higher than that of the model group（ P〈0. 01）. Inflammatory cells were lower in baicalin group than that in the model group. Conclusion： Baicalin can treat pulmonary fibrosis through reducing the expressions of TNF-α,IL-1β and MDA and increasing the activity of SOD in lung tissue. That is probably the mechanism of baicalin protecting pulmonary tissues.

关 键 词：黄芩苷 肺纤维化 炎症细胞 氧化应激 

分 类 号：R285.5[医药卫生—中药学]