Hydrogen sulfide supplement preserves mitochondrial function of retinal ganglion cell in a rat glaucoma model
Hydrogen sulfide supplement preserves mitochondrial function of retinal ganglion cell in a rat glaucoma model
复制标题
补充硫化氢可保护大鼠青光眼模型中视网膜神经节细胞的线粒体功能
DOI：
10.1007/s00441-022-03640-x
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发表时间：
2022-05
影响因子：
3.6
通讯作者：
Yisheng Zhong
中科院分区：
文献类型：
--
作者：
Shouyue Huang;Ping Huang;Huan Yu;Junjue Chen;Xiaohong Liu;Jing Wang;Xi Shen;Yisheng Zhong
青光眼是一种以视网膜神经节细胞（retinal ganglion cells，RGC）逐渐丧失为特征的视觉系统神经退行性疾病。鉴于视网膜神经节细胞线粒体功能障碍与青光眼的病理机制密切相关，而硫化氢（H2S）参与了青光眼的发病机制，并在恢复其他神经元线粒体功能方面显示出良好的潜力，作者旨在通过大鼠青光眼模型研究H2S对视网膜神经节细胞线粒体功能的影响。采用前房注射交联水凝胶法建立慢性高眼压（COH）大鼠模型，选用硫氢化钠（NaHS）作为H2S供体，通过腹腔注射对大鼠进行治疗。4周后，用免疫淘洗法从受试大鼠中分离RGCs，并通过线粒体膜电位（MMP）、线粒体通透性转换孔（MPTP）开放、细胞内Ca 2+水平、活性氧（ROS）水平和细胞溶质细胞色素C分布的评价。结果表明，H_2S可明显改善实验性青光眼视网膜神经节细胞线粒体功能，表现为稳定MMP，缓解MPTP开放，促进细胞内Ca ~（2+）止血，减少ROS积聚，抑制细胞色素C释放。我们的研究提示，H2S对视网膜神经节细胞线粒体功能的保护可能在青光眼神经病变中起关键作用，值得进一步深入研究，以利于青光眼治疗的发展。
Glaucoma is a neurodegenerative disease of visual system characterized by gradual loss of retinal ganglion cells (RGC). Since mitochondrial dysfunction of RGC is significantly involved in the pathological mechanisms of glaucoma, and hydrogen sulfide (H2S) takes part in the pathogeny of glaucoma and shows promising potential in restoring mitochondrial function in other neurons, the authors aimed to investigate the impact of H2S on mitochondrial function of RGC with a rat glaucoma model. An established chronic ocular hypertension (COH) rat model induced by injection of cross-linking hydrogel into anterior chamber was adopted, and a H2S donor, sodium hydrosulfide (NaHS), was selected to treat rats through intraperitoneal injection. After a period of 4 weeks, RGCs were isolated from the subjected rats with an immunopanning method and went through evaluations of mitochondrial membrane potential (MMP), mitochondrial permeability transition pore (MPTP) opening, intracellular Ca2 + level, reactive oxygen species (ROS) level, and cytosolic Cytochrome C distribution. The results showed that the mitochondrial function of RGC in experimental glaucoma was markedly improved by H2S supplement, being presented as stabilization of MMP, alleviation of MPTP opening, improvement of intracellular Ca2+ hemostasis, reduction of ROS accumulation, and inhibition of Cytochrome C release. Our study implicated that preservation of mitochondrial function by H2S probably plays a key role in protecting RGC in the context of glaucomatous neuropathy, and it is worth further deepgoing research to benefit the development of glaucoma treatment.
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影响因子：
--
作者：
Shefa U;Kim MS;Jeong NY;Jung J
通讯作者：
Jung J
DOI：
10.1126/science.1162667
发表时间：
2008-10-24
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Yang G;Wu L;Jiang B;Yang W;Qi J;Cao K;Meng Q;Mustafa AK;Mu W;Zhang S;Snyder SH;Wang R
通讯作者：
Wang R
影响因子：
6.1
作者：
Rubaiya Tabassum;N. Y. Jeong;Junyang Jung
通讯作者：
Rubaiya Tabassum;N. Y. Jeong;Junyang Jung
影响因子：
1.7
作者：
E. Erdem;A. Williams;Sarah Kuchar;M. Waisbourd;G. Spaeth
通讯作者：
E. Erdem;A. Williams;Sarah Kuchar;M. Waisbourd;G. Spaeth
影响因子：
2.2
作者：
W. Ju;Keun-Young Kim;Karen X. Duong-Polk;J. Lindsey;Mark Ellisman;R. Weinreb
通讯作者：
W. Ju;Keun-Young Kim;Karen X. Duong-Polk;J. Lindsey;Mark Ellisman;R. Weinreb