摘要
目的研究黄芩苷对FM1肺炎小鼠肺组织细胞凋亡FAS/FAS-L系统的影响,探索黄芩苷抗流感病毒感染机制。方法制备小鼠甲型流感病毒性肺炎模型,通过死亡保护实验确定黄芩苷的最小有效浓度,TUNEL法观察小鼠肺组织细胞凋亡情况,RT-PCR技术检测肺组织FAS(CD95)、FAS-L(CD178)、Caspase-3 mRNA表达,Western blot方法测定肺组织FAS、FAS-L、Caspase-3蛋白表达。结果与模型组相比,黄芩苷187.5、375 mg.kg-1剂量均能明显降低肺组织细胞凋亡率,明显降低肺组织FAS、FAS-L及Caspase-3 mRNA和蛋白的表达(P<0.05)。结论黄芩苷能够明显抑制FM1肺炎小鼠肺组织细胞的凋亡,其可能通过影响细胞凋亡受体途径FAS/FAS-L系统而发挥抗流感病毒感染作用。
Aim To investigate the effects of BAI on cell apoptosis FAS/FAS-L system of pneumonia mice lung tissue infected with FM1,and to explore BAI＇s mechanism of anti-influenza virus infection.Methods The model of mouse influenza virus pneumonia was prepared.BAI minimal effective concentration was determined by death protection experiment;TUNEL was applied to detect cell apoptosis of lung tissue;RT-PCR was adopted to determine the mRNA expressions of FAS（CD95）,FAS-L（CD178）,and Caspase-3;Western blot was used to determine the protein expressions of FAS,FAS L,and Caspase-3.Results Compared with the model,BAI,at doses 187.5 mg·kg-1 and 375 mg·kg-1,could obviously reduce cell apoptotic rate and significantly cut down mRNA and protein expressions of FAS,FAS-L,and Caspase-3（P0.05）.Conclusions BAI can obviously inhibit cell apoptosis FAS/FAS-L system of lung tissue infected with FM1.It may affect cell apoptosis receptor pathway to play functions of anti-influenza virus infection.
出处
《中国药理学通报》
CAS
CSCD
北大核心
2011年第11期1555-1559,共5页
Chinese Pharmacological Bulletin
基金
国家自然科学基金资助项目(No30772872)
