期刊文献+

雄附散对抗博莱霉素诱导的大鼠肺间质纤维化的作用机制 被引量:3

Role of Xiongfusan in preventing bleomycin-induced pulmonary fibrosis
下载PDF
导出
摘要 目的探讨雄附散对大鼠肺间质纤维化干预的机制。方法将70只SD大鼠随机分为正常组,假手术组,模型组,醋酸泼尼松组(5.6mg/kg),雄附散高、中、低剂量组(1.4g/kg、0.7g/kg、0.35g/kg)。各组大鼠于造模后第2天开始连续4周灌胃(ig),给予生理盐水(0.014L/kg)或相应药物(0.014L/kg),28d后取右中肺组织进行HE染色和Masson染色及MDA含量、SOD和GSH-PX活性测定。结果HE染色和Masson染色均提示雄附散高剂量组肺组织无明显形态学改变,肺组织中SOD和GSH-PX酶活性明显高于其他各组(P<0.01),MDA含量明显低于各药物干预组(P<0.01)。结论雄附散可能通过提高受损组织中抗氧化酶活性水平来对抗肺组织纤维化过程。 Objective To study the role of Xiongfusan in preventing bleomycin-induced pulmonary fibrosis. Methods Seventy SD rats were randomly divided into blank control group, sham-operation group, model group, prednisone treatment group(5.6mg/kg), and 3 Xiongfusan treatment groups (1.4g/kg, 0.7g/kg and 0.35g/kg). Rats received normal saline (0.014L/kg) and corresponding drugs (0.014L/kg) respectively from day 2 after gastric gavage of bleomycin, once a day for 4 weeks. MDA level and enzyme activity of SOD and GSH-PX were measured in tissues taken from the right and middle lung stained with HE and Masson stain 28 days after treatment. Results HE and Masson staining showed no obvious morphologic changes in lung tissues of the high dose Xiongfusan group. The enzyme activity of SOD and GSH-PX was significantly higher in the high dose Xiongfusan group than in the medium and low dose Xiongfusan treatment groups (P〈0.01). The MDA level was obviously lower in Xiongfusan treatment groups than in other groups (P〈0.01). Conclusion Xiongfusan can prevent bleomycin-induced pulmonary fibrosis by increasing the expression of antioxidant enzymes in injured lung tissues.
出处 《军医进修学院学报》 CAS 2010年第1期67-68,74,共3页 Academic Journal of Pla Postgraduate Medical School
基金 "十一五"军队中医药重大临床攻关课 (2006011003)~~
关键词 雄附散 肺纤维化 抗氧化剂 酶类 Xiongfusan Pulmonary Fibrosis Antioxidants Enzymes
  • 相关文献

参考文献5

二级参考文献40

  • 1胡一鸿,牛健康.超氧化物歧化酶研究进展[J].生物学教学,2005,30(1):2-4. 被引量:58
  • 2Kim K, Lu Z,Hay ED. Direct evidence for a role of beta-catenin/LEF-1 signaling pathway in induction of EMI[ J]. Cell Biol Int ,2002,26(5) : 463 - 476
  • 3Masszi A ,Fan L, Rosivall L, et al. Integrity of cell-cell contacts is a critical regulator of TGF-bcta 1-induced epit helial-to-myofibroblast transition:role for beta-catenin[J] .Am J Pat hol,2004,165(6) :1955- 1967
  • 4Pongraez JE, Stokley RA. Wnt signaling in lung development and diseases[J], Respir Res ,2006,1 (7) : 15
  • 5Ludwicka-Bradlwy A, Bogat kevieh G, Silver RM. Thrombin-mφdiated cellular events in pulmonary fibrosis associated with systemic sclerosis (scleroderma) [ J]. Clin Rheumatol, 2004,22 (3 Supp133) : 38 - 46
  • 6Kubo H, N akayama K, Yanai M, et al. Anticoagulant therapy for idiopathic pulmonary fibrosis[J]. Chest,2005,128(3) : 1475 - 1482
  • 7Maher TM, Wells AU, Laurent GJ. Idiopathic pulmonary fibrosis: multiple causes and multiple mechanisms? [ J ]. Eur Respir J, 2007, 30 ( 5 ) : 835 - 839
  • 8Selman M, Thannickal VJ, Pardo A, et al. Idiopathic pulmonary fibrosis: pathogenesis and therapeutic approaches [ J ]. Dross, 2004,64 ( 4 ) : 405 - 430
  • 9King TE Jr, SchWarz ML, Brown K, et al. Idiopathic pulmonary fibrosis: relationship between histopathologic features and mortality[J] .Am J Respir Crit Care Med, 2001,164(6) : 1025 - 1032
  • 10Cool CD, Groshong SD, Rai PR, et al. Fibroblast foci are not discrete sites of lung injury or repair: the fibroblast reticuhm[ J] .Am J Respir Crit Care Med, 2006,174(6):654-658

共引文献61

同被引文献31

引证文献3

二级引证文献11

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