期刊文献+

雷公藤多甙对哮喘大鼠血清及肺组织NO含量和总抗氧化能力的影响 被引量:12

Effect of tripterygium wilfordii on nitric oxide and total antioxidative capability in serum and lung tissues of asthma rats
下载PDF
导出
摘要 目的观察雷公藤多甙对哮喘大鼠血清及肺组织一氧化氮(NO)含量和总抗氧化能力(T-AOC)的影响。方法雄性Wistar大鼠36只,体重200g左右,随机分为对照组、哮喘组和雷公藤干预组。测量各组大鼠血清及肺组织NO含量和T-AOC。结果哮喘组大鼠血清及肺组织NO含量显著高于对照组和雷公藤干预组(均P<0.05),而雷公藤干预组显著高于对照组(均P<0.05)。哮喘组大鼠血清及肺组织T-AOC较对照组和雷公藤干预组降低,差异有统计学意义(均P<0.05),但雷公藤干预组显著低于对照组(P<0.05)。结论雷公藤多甙能提高哮喘大鼠体内的抗氧化能力,这种作用可能是通过抑制哮喘大鼠气道NO的合成实现的。 Objective To explore the effect of tripterygium wilfordii(TW) on nitric oxide and total antioxidative capability in serum and lung tissues of asthma rats. Methods Thirty-six Wistar male rats were randomly divided into control group,asthma group and TW treated group. NO concentration and total antioxidative capability in serum and lung tissues of asthma rats were detected. Results The NO concentration in serum and lung tissues in asthma group were significantly higher than in control group and TW treated group(P 〈0.05),but total antioxidative capability in asthma group were significantly lower than in control group and TW treated group(P〈0.05). The NO concentration in serum and lung tissues in TW treated group were higher than in control group (P 〈0.05), while total antioxidative capability in serum and lung tissues were significantly lower than in control group( P 〈 0.05). Conclusion Tripterygium wilfordii may enhance antioxidative capability in asthma rats through reducing NO concentration.
出处 《山西医科大学学报》 CAS 2008年第4期311-313,共3页 Journal of Shanxi Medical University
关键词 雷公藤多甙 哮喘 一氧化氮 总抗氧化能力 tripterygium wilfordii asthma nitric oxide total antioxidative capability
  • 相关文献

参考文献9

二级参考文献24

  • 1秦凤华,谢蜀生,龙振洲.雷公藤总甙免疫抑制作用的机制[J].中国药理学通报,1991,7(6):433-436. 被引量:18
  • 2张崇璞,吕燮余,马鹏程,陈沄,张永刚,言政,陈国芳,郑启泰,贺存恒,于德泉.雷公藤叶中二萜化合物的研究[J].药学学报,1993,28(2):110-115. 被引量:20
  • 3Donna E,Davies PHD,James W,et al.Airway remodeling in asthma:new insight [J].J Allergy Clin Immunol,2003,111:215- 225.
  • 4Holgate ST.Asthma:more than an inflammatory disease[J].Curr Opin Allergy Clin Immunol,2002,2:27 - 29.
  • 5Yang Y,Bin W,Aksoy MO,et al.Regulation of interleukin1beta and interleukin-1beta inhibitor release by human airway epithelial cells[J].Eur Respir J,2004,24:360 - 366.
  • 6Lappalainen V,Whitsett JA,Wert SE,et al.Interleukin-1beta cause pulmonary inflammation,emphysema,and airway remodeling in the adult murine lung[J].Am J Respir Cell Mol Boil,2005,32:311 - 318.
  • 7Holgate ST,Holloway J,Wilson S,et al.Epithelial-mesenchymal communication in the pathogenesis of chronic asthma [J].Proc Am Thorac Soc,2004,1 :93 - 98.
  • 8Vignola AM,Chane P,Chiappara G,et al.Transforming growth factor-beta expression in mucosal biopsies in asthma and chronic bronchitis[J].Am J Kespir Crit Med,1997,156:591 - 599.
  • 9Vanacker NJ,Palmmans ELS,Kips JC,et al.Fluticasone inhibits but does not reverse allergen-induced structural airway changes[J].Am J Respir Crit Care Med,2001,163:674 - 667
  • 10Holgate ST,Holloway J,Wilson S,et al.Epithelial-mesenchymal interation in the pathogenesis of athma[J].J Allergy Clin Immunol,2000,105:193 - 204.

共引文献55

同被引文献157

引证文献12

二级引证文献53

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部