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Remote Ischemic Preconditioning Protects Retinal Photoreceptors: Evidence From a Rat Model of Light-Induced Photoreceptor Degeneration.远程缺血预处理对视网膜光感受器具有保护作用:来自光诱导光感受器变性大鼠模型的证据。
Invest Ophthalmol Vis Sci. 2016 Oct 1;57(13):5302-5313. doi: 10.1167/iovs.16-19361.
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Determinants of the Efficacy of Cardiac Ischemic Preconditioning: A Systematic Review and Meta-Analysis of Animal Studies.心脏缺血预处理疗效的决定因素:动物研究的系统评价与荟萃分析
PLoS One. 2015 Nov 18;10(11):e0142021. doi: 10.1371/journal.pone.0142021. eCollection 2015.
3
Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents.远程肢体缺血预处理:一种在啮齿动物中的神经保护技术。
J Vis Exp. 2015 Jun 2(100):e52213. doi: 10.3791/52213.
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Induction of ischemic tolerance as a promising treatment against diabetic retinopathy.诱导缺血耐受作为治疗糖尿病视网膜病变的一种有前景的方法。
Neural Regen Res. 2014 Sep 1;9(17):1581-4. doi: 10.4103/1673-5374.141782.
5
Hepatocyte growth factor promotes long-term survival and axonal regeneration of retinal ganglion cells after optic nerve injury: comparison with CNTF and BDNF.肝细胞生长因子促进视神经损伤后视网膜神经节细胞的长期存活和轴突再生:与睫状神经营养因子和脑源性神经营养因子的比较。
CNS Neurosci Ther. 2014 Oct;20(10):916-29. doi: 10.1111/cns.12304. Epub 2014 Jul 3.
6
COX-2 inhibition improves retinal function in rats' ischemic eyes.环氧化酶-2抑制可改善大鼠缺血性眼睛的视网膜功能。
J Ocul Pharmacol Ther. 2014 Oct;30(8):634-41. doi: 10.1089/jop.2013.0150. Epub 2014 Jun 17.
7
Remote ischemic postconditioning promotes the survival of retinal ganglion cells after optic nerve injury.远程缺血后处理促进视神经损伤后视网膜神经节细胞的存活。
J Mol Neurosci. 2013 Nov;51(3):639-46. doi: 10.1007/s12031-013-0036-2. Epub 2013 Jun 5.
8
Ischemic tolerance protects the rat retina from glaucomatous damage.缺血耐受可保护大鼠视网膜免受青光眼损伤。
PLoS One. 2011;6(8):e23763. doi: 10.1371/journal.pone.0023763. Epub 2011 Aug 24.
9
Induction of heat shock proteins 27 and 72 in retinal ganglion cells after acute pressure-induced ischaemia.急性压力诱导缺血后视网膜神经节细胞中热休克蛋白27和72的诱导表达
Clin Exp Ophthalmol. 2009 Apr;37(3):299-307. doi: 10.1111/j.1442-9071.2009.02032.x.
10
Opioid receptor-activation: retina protected from ischemic injury.阿片受体激活:视网膜免受缺血性损伤。
Invest Ophthalmol Vis Sci. 2009 Aug;50(8):3853-9. doi: 10.1167/iovs.08-2907. Epub 2009 Mar 25.

通过诱导缺血预处理保护视网膜神经节细胞免受视神经损伤。

Protection of retinal ganglion cells against optic nerve injury by induction of ischemic preconditioning.

作者信息

Liu Xia, Liang Jiu-Ping, Sha Ou, Wang Song-Juan, Li Heng-Guo, Cho Eric Y P

机构信息

Medical Imaging Center, the First Affiliated Clinical Hospital of Jinan University, Guangzhou 510632, Guangdong Province, China.

School of Biomedical Sciences, the Chinese University of Hong Kong, Shatin, Hong Kong 999077, China.

出版信息

Int J Ophthalmol. 2017 Jun 18;10(6):854-861. doi: 10.18240/ijo.2017.06.05. eCollection 2017.

DOI:10.18240/ijo.2017.06.05
PMID:28730074
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5515167/
Abstract

AIM

To explore if ischemic preconditioning (IPC) can enhance the survival of retinal ganglion cells (RGCs) after optic nerve axotomy.

METHODS

Twenty-four hours prior to retinal ischemia 60min or axotomy, IPC was applied for ten minutes in groups of (=72) animals. The survival of RGCs, the cellular expression of heat shock protein 27 (HSP27) and heat shock protein 70 (HSP70) and the numbers of retinal microglia in the different groups were quantified at 7 and 14d post-injury. The cellular expression of HSP27 and HSP70 and changes in the numbers of retinal microglia were quantified to detect the possible mechanism of the protection of the IPC.

RESULTS

Ten minutes of IPC promoted RGC survival in both the optic nerve injury (IPC-ONT) and the retinal ischemia 60min (IPC-IR60) groups, examined at 7d and 14d post-injury. Microglial proliferation showed little correlation with the extent of benefit effects of IPC on the rescue of RGCs. The number of HSP27-positive RGCs was significantly higher in the IPC-ONT group than in the sham IPC-ONT group, although the percentage of HSP27-positive RGCs did not significantly differ between groups. For the IPC-IR60 group, neither the number nor the percentage of the HSP27-positive RGCs differed significantly between the IPC and the sham-operated groups. The number of HSP70-positive RGCs was significantly higher for both the IPC-ONT and the IPC-IR60 experimental groups, but the percentages did not differ.

CONCLUSION

The induction of IPC enhances the survival of RGCs against both axotomy and retinal ischemia.

摘要

目的

探讨缺血预处理(IPC)能否提高视神经切断术后视网膜神经节细胞(RGCs)的存活率。

方法

在视网膜缺血60分钟或视神经切断术前24小时,对(=72)只动物分组进行10分钟的IPC处理。在损伤后7天和14天,对不同组中RGCs的存活情况、热休克蛋白27(HSP27)和热休克蛋白70(HSP70)的细胞表达以及视网膜小胶质细胞数量进行定量分析。对HSP27和HSP70的细胞表达以及视网膜小胶质细胞数量的变化进行定量分析,以检测IPC保护作用的可能机制。

结果

在损伤后7天和14天检查发现,10分钟的IPC可促进视神经损伤组(IPC-ONT)和视网膜缺血60分钟组(IPC-IR60)中RGCs的存活。小胶质细胞增殖与IPC对RGCs挽救的有益作用程度几乎没有相关性。IPC-ONT组中HSP27阳性RGCs的数量显著高于假手术IPC-ONT组,尽管各组间HSP27阳性RGCs的百分比无显著差异。对于IPC-IR60组,IPC组和假手术组之间HSP27阳性RGCs的数量和百分比均无显著差异。IPC-ONT和IPC-IR60实验组中HSP70阳性RGCs的数量均显著更高,但百分比无差异。

结论

IPC的诱导可提高RGCs抵抗切断术和视网膜缺血的存活率。