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己酮可可碱对1型糖尿病的免疫干预治疗 被引量：2

The Intervention Effect of Pentoxifylline on Type 1 Diabetes
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作者 施念玮 吴艺捷
机构地区 上海交通大学附属第一人民医院内分泌科
出处 《复旦学报（医学版）》 CAS CSCD 北大核心 2005年第5期622-624,共3页 Fudan University Journal of Medical Sciences
基金 上海市卫生局科技发展基金资助课题(01439)
关键词 1型糖尿病 己酮可可碱 干预治疗
分类号 R587 [医药卫生—内分泌]
  • 相关文献

参考文献25

  • 1Pozzillip P,Pitocco d,Visalli N,et al. Rapid communication:No effect of oral insulin on residual beta-cell function in recent-onset type I diabetes (The IMDIAB Ⅶ ). Diabetologia ,2000,43:1000.
  • 2Schatz DA,Birgley PJ. Up date on major trails for the prevention of type 1 diabetes mellitus: The american Diabetes Prevention Trial (DPT-1) and the European Nicotinamide Diabetes Intervention Trial( ENDIT). J Pediatr Endocrnol Metab , 2001,14, (Suppll):619.
  • 3Philps JC,Scheen AJ. Info-Congress. Study of prevention of type 1 diabetes with nicotinamide: positive lessons of a negative clinical trial (ENDIT). Rev Med Liege ,2002,57:672.
  • 4Abdel-Salam OME,Baiuomy AR,El-Shenawy SM,et al. The antiinflammatory effects of the phosphodiesterase inhibitor pentoxifylline in the rat. Pharmacol Res ,47,331.
  • 5Liang L,Beshay E, et al. The Phosphodiesterase Inhibitors Pentoxifylline and Rolipram Prevent Diabetes in NOD Mice. Diabetes,1998,47:570.
  • 6Stosic-Grujicic SD, Maksimovic DD, Stojikovic MB, et al. Pentoxifylline prevents autoimmune mediated inflammation in low dose streptozotocin induced diabetes. Dev Immunol,2001,8(3-4) :213.
  • 7陈改玲,党爱民,刘国仗.T淋巴细胞与1型糖尿病[J].国外医学（内分泌学分册）,2001,21(6):299-301. 被引量：3
  • 8何军华,兰丽珍,张志利,李昭瑛.己酮可可碱对NOD小鼠1型糖尿病的影响[J].中华内分泌代谢杂志,2002,18(5):388-390. 被引量：5
  • 9郭志勇,李保春,袁伟杰,崔若兰.细胞间粘附分子-1在腹膜炎症过程中的作用及己酮可可碱的保护效应[J].中国血液净化,2003,2(6):319-321. 被引量：3
  • 10Giembycz MA, Corrigon CJ, Newton R, et al. Identification of cyclic AMP phosphoiesterases 3,4 and 7 in human CD4+ and CD8+ T-lymphocytea: role in regulating prolieration and the biosynthesis of interleukin-2. Br J pharmacol , 1996,118:1945.

二级参考文献41

  • 1裴的善.己酮可可碱的临床新用途[J].新医学,1995,26(4):205-206. 被引量：3
  • 2[1]Obrien BA,Harmon BV,Cameron DP,et al.Apoptosis is the mode of β-cell responsible for the development of IDDM in the nonbese diabetic (NOD) mouse[J].Diabetes,1997,46:750～757.
  • 3[2]Lamhamedi-Cherradi SE,Luan JJ,Eloy L,et al.Resistance of T-cell to apoptosis in autoimmune diabetic (NOD) mice is increased early in life and is associated with dysregulated expression of Bcl-x[J].Diabetologia,1998,41:178～184.
  • 4[3]Trudeau JD,Dutz JP,Arany E,et al.Neonatal cell apoptosis:a trigger for autoimmune diabetes[J].Diabetes,2000,49:1～79.
  • 5[4]Su X,Hu Q,Kristan JM,et al.Significant role for Fas in the pathogenesis of autoimmune diabetes[J].J Immunol,2000,164:2 523～2 532.
  • 6[5]Suarez-Pinzon W,Sorensen O,Bleackley RC,et al.β-cell destruction in NOD mice correlates with Fas (CD95) expression on β-cells and proinflammatory cytokine expression in islets[J].Diabetes,1999,48:21～28.
  • 7[6]Loweth AC,Williams GT,James RFL,et al.Human islets of langerhans express Fas ligand and undergo apoptosis in response to interleukin-1 β and Fas ligation[J].Diabetes,1998,47:727～732.
  • 8[7]Chervonsky AV,Wang Y,Wong FS,et al.The role of Fas in autoimmune diabetes[J].Diabetes Cell,1997,89:17～24.
  • 9[8]Kim YH,Kim S,Kim KA,et al.Apoptosis of pancreatic β-cells detected in accelerated diabetes of NOD mice:no role of Fas-Fas ligand interaction in autoimmune diabetes[J].Eur J Immunol,1999,29:455～465.
  • 10[9]Stephens LA,Thomas HE,Ming L,et al.Tumor necrosis factor-α-activated cell death pathways in NIT-1 insulinoma cells and primary pancreatic β-cells[J].Endocrinology,1999,140:3 219～3 227.

共引文献9

同被引文献28

引证文献2

二级引证文献4

复旦学报（医学版）
2005年 第5期

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