中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2018, Vol. 13 ›› Issue (11): 2014-2021.doi: 10.4103/1673-5374.239450

• 原著:视神经损伤修复保护与再生 • 上一篇    下一篇

牛磺酸通过抗氧化作用保护内皮素-1诱导的视网膜和视神经损伤

  

  • 收稿日期:2018-08-09 出版日期:2018-11-15 发布日期:2018-11-15
  • 基金资助:

    这项研究获得了Universiti Teknologi MARA的资助，资助号为600-IRMI / DANA5 / 3 / BESTARI（006/2017）

Taurine protects against retinal and optic nerve damage induced by endothelin-1 in rats via antioxidant effects

Natasha Najwa Nor Arfuzir1, Renu Agarwal1, Igor Iezhitsa1, 2, Puneet Agarwal3, Sabrilhakim Sidek1, Nafeeza Mohd Ismail1   

  1. 1 Center for Neuroscience Research, Faculty of Medicine, Universiti Teknologi MARA Sungai Buloh Campus, Selangor, Malaysia
    2 Volgograd State Medical University, Research Institute of Pharmacology, Volgograd, Russia
    3 Faculty of Medicine, International Medical University, IMU Clinical School, Seremban, Malaysia
  • Received:2018-08-09 Online:2018-11-15 Published:2018-11-15
  • Contact: Renu Agarwal, PhD, renuag02@gmail.com
  • Supported by:

    This study obtained the financial support by Universiti Teknologi MARA under grant No. 600-IRMI/DANA5/3/BESTARI (006/2017).

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摘要：

内皮素1是一种有效的血管收缩剂，参与青光眼的视网膜血管失调和氧化应激。牛磺酸是一种天然存在的游离氨基酸，有神经保护作用，且具备抗氧化特性；然而其对内皮素1诱导的视网膜和视神经损伤作用尚不明确。因此实验将2.5 nM 内皮素1玻璃体内注射于来源于马来西亚MARA大学医学院实验动物护理所的SD大鼠，并将320 nM牛磺酸作为治疗前，治疗后或同时施用的药物进行玻璃体内注射。牛磺酸注射后7天进行HE和甲苯胺蓝染色以观察视网膜和视神经形态，并进行半胱天冬酶3免疫染色评估细胞凋亡，以ELISA法检测视网膜超氧化物歧化酶，过氧化氢酶，谷胱甘肽和丙二醛水平来估计视网膜氧化还原状态。结果显示，牛磺酸治疗组的视网膜和视神经形态明显改善，且视网膜氧化应激降低，尤以牛磺酸预处理组作用最为明显。免疫染色显示牛磺酸预处理大鼠凋亡的视网膜细胞数量显著减少。说明牛磺酸在预防由内皮素1诱导的视网膜和视神经损害方面作用显著，该作用可能与降低氧化应激水平有关。

orcid:0000-0002-3050-7449(Renu Agarwal)

关键词: 内皮素-1, 视网膜, 视神经, 牛磺酸, 氧化应激, 神经再生

Abstract:

Endothelin-1 (ET-1), a potent vasoconstrictor, is involved in retinal vascular dysregulation and oxidative stress in glaucomatous eyes. Taurine (TAU), a naturally occurring free amino acid, is known for its neuroprotective and antioxidant properties. Hence, we evaluated its neuroprotective properties against ET-1 induced retinal and optic nerve damage. ET-1 was administered intravitreally to Sprague-Dawley rats and TAU was injected as pre-, co- or post-treatment. Animals were euthanized seven days post TAU injection. Retinae and optic nerve were examined for morphology, and were also processed for caspase-3 immunostaining. Retinal redox status was estimated by measuring retinal superoxide dismutase, catalase, glutathione, and malondialdehyde levels using enzyme-linked immuosorbent assay. Histopathological examination showed significantly improved retinal and optic nerve morphology in TAU-treated groups. Morphometric examination showed that TAU pre-treatment provided marked protection against ET-1 induced damage to retina and optic nerve. In accordance with the morphological observations, immunostaining for caspase showed a significantly lesser number of apoptotic retinal cells in the TAU pre-treatment group. The retinal oxidative stress was reduced in all TAU-treated groups, and particularly in the pre-treatment group. The findings suggest that treatment with TAU, particularly pre-treatment, prevents apoptosis of retinal cells induced by ET-1 and hence prevents the changes in the morphology of retina and optic nerve. The protective effect of TAU against ET-1 induced retinal and optic nerve damage is associated with reduced retinal oxidative stress.

Key words: endothelin-1, retina, optic nerve, taurine, oxidative stress