RELEVANT VARIATIONS AND NEUROPROTECIVE EFFECT OF HYDROGEN SULFIDE IN A RAT GLAUCOMA MODEL
RELEVANT VARIATIONS AND NEUROPROTECIVE EFFECT OF HYDROGEN SULFIDE IN A RAT GLAUCOMA MODEL
复制标题
硫化氢在大鼠青光眼模型中的相关变化及神经保护作用
DOI:
10.1016/j.neuroscience.2016.11.019
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发表时间:
2017-01-26
期刊:
影响因子:
3.3
通讯作者:
Zhong, Yisheng
中科院分区:
文献类型:
--
作者:
Huang, Shouyue;Huang, Ping;Zhong, Yisheng
Glaucoma is an irreversible and blinding neurodegenerative disease of the eye, and is characterized by progressive loss of retinal ganglion cells (RGCs). Since endogenous hydrogen sulfide (H2S) was reported to be involved in neurodegeneration in the central nervous system, the authors aimed to develop a chronic ocular hypertension (COH) rat model simulating glaucoma and therein test the H2S level together with the retinal protein expressions of related synthases, and further investigated the effect of exogenous H2S supplement on RGC survival. COH rat model was induced by cross-linking hydrogel injection into anterior chamber, and the performance of the model was assessed by intraocular pressure (IOP) measurement, RGC counting and retinal morphological analysis. Endogenous H2S level was detected along with the retinal protein expressions of H2S-related synthases cystathionine beta-synthase (CBS), cystathionine gamma-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST) in the COH rats. Retinal H2S level and RGC survival were evaluated again after NaHS (a H2S donor) treatment in the COH rats. The results showed that the COH model succeeded in simulating glaucoma features, and retinal H2S level decreased significantly when the retinal protein expressions of CBS, CSE and 3-MST were downregulated generally in the COH rats. Furthermore, the decrease of retinal H2S level and loss of RGCs were both improved by NaHS treatment in experimental glaucoma, without obvious variation of IOP. Our study revealed that the intracameral injection of cross linking hydrogel worked efficiently in modeling glaucoma, and H2S had protective effect on RGCs and might be involved in the pathological mechanism of glaucomatous neuropathy. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.