世界中医药
文章摘要
引用本文:陆远,赵霞.固本防哮饮对哮喘缓解期小鼠肺组织内质网应激相关凋亡基因CRT和EDEM的影响[J].世界中医药,2016,(09):.  
固本防哮饮对哮喘缓解期小鼠肺组织内质网应激相关凋亡基因CRT和EDEM的影响
Effects of Gubenfangxiao Decoction on Lung Tissue ER Stress-associated Apoptotic Genes CRT and EDEM in Murine Asthmatic Remission Models
投稿时间:2016-09-09  
DOI:10.3969/j.issn.1673-7202.2016.09.003
中文关键词:  固本防哮饮  哮喘缓解期  蛋白质未折叠反应  CRT  EDEM
English Keywords:Guben Fangxiao Decoction  Asthma remission  Unfolded protein response  CRT  EDEM
基金项目:国家自然科学基金项目(编号:81473723)
作者单位
陆远,赵霞 南京中医药大学江苏省儿童呼吸疾病(中医药)重点实验室南京210023 
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中文摘要:
      目的:探讨中药复方固本防哮饮对哮喘缓解期小鼠肺组织内质网应激相关的凋亡基因CRT和EDEM的影响。方法:结合前期研究采用卵蛋白(OVA)致敏和OVA-呼吸道合胞病毒(RSV)联合诱导激发BALB/c雌性小鼠,建立哮喘缓解期动物模型,随机分为正常组,模型组,固本防哮饮低、中、高剂量组,孟鲁司特钠组及地塞米松组。Real-time PCR法检测肺组织中EDEM和CRT mRNA表达水平。结果:模型组小鼠肺组织中CRT表达显著高于正常组(P<0.05);固本防哮饮高、中剂量组,孟鲁司特钠组及地塞米松组小鼠肺组织中CRT mRNA表达均显著低于模型组(P<0.05),而EDEM在各组中表达无统计学意义(P>0.05)。结论:固本防哮饮防治哮喘减轻慢性气道炎性反应的作用机制可能是通过抑制蛋白质未折叠反应相关的凋亡基因CRT表达所致。
English Summary:
      To explore the effects of Gubenfangxiao Decoction(GBFXD)on lung tissue ER stress-associated apoptotic gene CRT and EDEM in murine asthma remission models.Methods:According to former studies,OVA sensitization and RSV-OVA were used for stimulation and inducement on BALB/c female mice to build animal asthma remission models,which were then randomly grouped into normal group,model group,GBFXD high dose group,GBFXD medium dose group,GBFXD low dose group,Montelukast Sodium group and Dexamethasone group.The mRNA levels of ER stress-associated apoptotic genes CRT and EDEM were detected via RT-PCR method.Results:The lung tissue CRT expression of the model group is significantly higher than that of the normal group(P<0.05); In GBFXD high dose group,GBFXD medium dose group,Montelukast Sodium group and Dexamethasone group,inhibited ER stress-associated apoptotic genes CRT were observed through the significant reduction of mRNA expressions after GBFXD treatment.(P<0.05)Conclusion:Guben Fangxiao Decoction significantly attenuates RSV-OVA-induced persistent airway inflammation in murine asthma remission model.These effects may be mediated,at least partially,by inhibiting the activation of ER stress-associated apoptotic genes CRT.
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