期刊文献+

视网膜神经节细胞损伤机制及神经保护药物研究进展 被引量:5

Retinal Ganglion Cells Injury Mechanisms and Neuroprotective Drug Research
下载PDF
导出
摘要 近年来,青光眼的研究焦点已转向神经保护。各种以不同的神经保护药物为基础的实验研究结果表明,神经保护治疗能减少视网膜神经节细胞的损害。针对引起视网膜神经节细胞死亡的不同机制及靶点已开发出多种不同来源的视网膜神经节细胞神经保护药物,这些药物通过多种分子机制及信号通路发挥作用,部分药物已进入临床研究阶段,并有望进入临床使用。 In recent years,the focus of glaucoma research has shifted toward neuroprotection,various neuroprotective drug-based approaches have been shown capable of reducing the death of retinal ganglion cells.In this review,several potential neuroprotective strategies were reviewed.Many of the approaches employ and manipulate the cell′s endogenous mechanism to promote the survival of RCGs.A list of neuroprotective agents are currently undergoing clinical and pre-clinical study.
作者 林莉 王玮
出处 《医学综述》 2009年第24期3745-3748,共4页 Medical Recapitulate
关键词 青光眼 视网膜神经节细胞 损伤机制 神经保护药物 Glaucoma Retinal ganglion cells Injury mechanism Neuroprotection
  • 相关文献

参考文献1

二级参考文献2

  • 1K. Adachi,S. Kashii,Hirokazu Masai,Mutsuaki Ueda,Chikako Morizane,Katsuyuki Kaneda,Toshiaki Kume,Akinori Akaike,Yoshihito Honda.Mechanism of the pathogenesis of glutamate neurotoxicity in retinal ischemia[J].Graefe’s Archive for Clinical and Experimental Ophthalmology.1998(10)
  • 2M. T. Droy-Lefaix.Effect of the antioxidant action of Ginkgo biloba extract (EGb 761) on aging and oxidative stress[J].AGE.1997(3)

共引文献6

同被引文献55

  • 1任历,于洪儒,王洪新.几种体外培养神经细胞缺氧模型效果的对比[J].辽宁医学院学报,2007,28(1):20-22. 被引量:8
  • 2Chen Y, Wang J J, Li J, Hosoya KI, Ratan R, Townes T, et al. Acti- vating transcription factor 4 mediates hyperglycaemia-induced endothelial inflammation and retinal vascular leakage through activation of STAT3 in a mouse model of type 1 diabetes [ J ]. Diabetologia ,2012 ,55 ( 9 ) :2533-2545.
  • 3Kusari J, Zhou SX, Padillo E, Clarke KG, Gil DW. Inhibition of vitreoretinal VEGF elevation and blood-retinal barrier break- down in streptozotocin-induced diabetic rats by brimonidine[J]. Invest Ophthalmol Vis Sci,2010,51(2) :1044-1051.
  • 4Liew G, Campbell S, Klein R, Klein BE, Sharrett AR, Cotch MF, et al. Ten-year longitudinal changes in retinal microvascular le- sions:the atherosclerosis risk in communities study [ J ]. Oph- thalmology,2011,118(8) :1512-1518.
  • 5Abbas A, Blandon J, Rude J, Elfar A, Mukherjee D. PPAR-γ ago- nist in treatment of diabetes: cardiovascular safety considera- tions [ J ]. Cardiovasc Hematol Agents Med Chem, 2012,10 ( 2 ) : 124-134.
  • 6Namvaran F, Azarpira N, Rahimi-Moghaddam P, Dabbaghmane- sh MH. Polymorphism of peroxisome proliferator-activated re-ceptor γ (PPARγ) Pro12Ala in the Iranian population: relation with insulin resistance and response to treatment with pioglita- zone in type 2 diabetes [ J ]. Eur J Pharmacol,2011,671 ( 1-3 ) : 1 - 6.
  • 7Sharma AK, Bharti S, Kumar R, Krishnamurthy B, Bhatia J, Ku- mari S, et al. Syzygium cumini ameliorates insulin resistance and β-cell dysfunction via modulation of PPAR, dyslipidemia, oxida- tive stress, and TNF-α in type 2 diabetic rats [J]. J Pharmacol Sci ,2012,119 ( 3 ) :205-213.
  • 8Shrestha RK. Ocular manifestations in diabetes, a hospital based prospective study [ J ]. Nepal Med Coil J, 2011,13 ( 4 ) : 254 -255.
  • 9Wong TY, Simo R, Mitchell P. Fenofibrate-a potential systemic treatment for diabetic retinopathy[ J]. Am J Ophthalmol, 2012, 154(1 ) :6-12.
  • 10Yang Y, Mao D, Chen X, Zhao L, Tian Q, Liu C, et al. Decrease in retinal neuronal cells in streptozotocin-induced diabetic mice[J]. Mol Vis ,2012,18 : 1411-1420.

引证文献5

二级引证文献27

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