期刊文献+

RA患者体内氧自由基水平的变化与应用血管活性肽的相关性 被引量:1

The interrelation between applying vasoactive peptide and change of OFR 1 level in RA patient
下载PDF
导出
摘要 目的:应用血管活性肽(商品名:脉炎康或栓必克,系沈阳荣达生物工程公司研制)治疗类风湿性关节炎(RA),观察其体内氧自由基与一系列指标的变化,并比较用药前后的相关关系。方法:取正常人25例为对照组,RA患者41例为治疗组,治疗组又随机分为单用非甾体抗炎药(NSAID)组和NSAID+脉炎康组,该2组患者用药前及用药10d后各采血一次。结果:治疗组比对照组,其红细胞内超氧化物歧化酶(SOD)明显升高,尤其NSAID+脉炎康组较单用NSAID组升高更显著(P<0.05);而过氧化脂质(LPO)明显下降,也较单用NSAID组下降更显著(P<0.05)。结论:证明该药物影响了红细胞内的氧自由基代谢,对治疗类风湿症起到了良好的效果,为类风湿的治疗开辟一条新途径。 Objective:Vasoactive peptied,a peptied extract was isolated from epithelium of human placenta vascular.To investigate its effects on RA.Methods:RA patients were divided into two groups by chance.One,the practice group,was administered vasoactive peptide and NSAIDs for 10 days.The other,practice Control group,was treated by NSAIDs oney for 10 days.Results:The results showed that the treatments of both groups are effective.The level of SOD in practice group was significantly higher than those in practice control group (P<0.05),LPO was significantly lower (P<0.05).Conclusions:We conclude that vasoactive peptide produce preferable effects to increase SOD,then reduce the level of OFR,inhibit the development of joint injury.And this is clinical potential in treatment of RA.
出处 《现代康复》 CSCD 1999年第4期410-412,共3页 Modern Rehabilitation
关键词 RA 氧自由基 血管活性肽 类风湿性关节炎 脉炎康 Vasoactive peptide Rheumatoid arthritis Oxygen free radicals
  • 相关文献

同被引文献14

  • 1怀善峰,陈东,高弘.腰椎间盘突出症手法治疗临床研究[J].现代康复,1999,3(1):45-46. 被引量:1
  • 2[2]KHATIB AM,SIEGFRIED G,QUINTERO M, et al.The mechanism of inhibition of DNA synthesis in articular chondrocytes from young and old rats by nitric oxide[J]. Nitric Oxide,1997, 1:218-225.
  • 3[3]BLANCO FJ,LOTZ M.IL-1-induced nitric oxide inhibits chondrocyte proliferation via PGE2[J].Exp Cell Res,1995, 218:319-325.
  • 4[4]SASAKI K,HATTORI T,FUJISAWA T, et al. Nitric oxide mediate interleuin-1-induced gene expression of matrix metalloproteinases and basic fibroblast growth factor in cultured rabbit articular chondrocytes[J].J Biochem,1998, 123:431-439.
  • 5[5]FRENKEL SR,CLANCY RM ,RICCI JL, et al.Effects of nitric oxide on chondrocyte migration, adhesion, and ytoskeletal assembly [J].Arthitis Rheum,1996, 39:1905-1912.
  • 6[6]BLANCO FJ,Ochs RL,SCHWARZ H, et al.Chondrocyte apoptosis induced by nitric oxide[J].Am J Pathol,1995, 146:75-85.
  • 7[7]CLANCY RM, ABRAMSON SB,Kohne C, et al.Nitric oxide attenuates cellular hexose monophosphate shunt response to oxidant in articular chondrocytes and acts to promote oxidant injury[J].J Cell Physiol,1997, 172, 183-191.
  • 8[8]CLANCY RM,REDISKE J,TANG X, et al.Outside-in signaling in the chondrocyte.Nitric oxide disrupts fibronectin-induced assembly of a subplasmalemmal actin /rho /focal adhesion kinase signaling complex[J].J Clin Invest,1997, 100:1789-1796.
  • 9[9]BIRD JL,WELLSs T,PLATT D, et al. IL-1 beta induces the degradation of equine articular catilage by a mechanism that is not mediated by nitric oxide[J].Biochem Biophys Res Commun,1997, 238:81-85
  • 10[10]MURRELL GA,JANG D,WILLIAMS RJ. Nitric oxide activates metalloprotease enzymes in articular cartilage[J].Biochem Biophys Res Commun,1995, 206(18):115-121.

引证文献1

二级引证文献1

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