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在链脲佐菌素诱导的Sprague-Dawley大鼠中,膳食补充牛磺酸通过减轻谷氨酸的兴奋性毒性来改善糖尿病视网膜病变。

Dietary taurine supplementation ameliorates diabetic retinopathy via anti-excitotoxicity of glutamate in streptozotocin-induced Sprague-Dawley rats.

作者信息

Yu Xiaoping, Xu Zhaoxia, Mi Mantian, Xu Hongxia, Zhu Jundong, Wei Na, Chen Ka, Zhang Qianyong, Zeng Kaihong, Wang Jian, Chen Fang, Tang Yong

机构信息

Department of Public Health, School of Preclinical Medicine, Chengdu Medical College, 601 Rongdu Road, Jinniu District, Chengdu 610081, China.

出版信息

Neurochem Res. 2008 Mar;33(3):500-7. doi: 10.1007/s11064-007-9465-z. Epub 2007 Aug 31.

Abstract

The purpose of this study was to investigate whether taurine ameliorate the diabetic retinopathy, and to further explore the underlying mechanisms. The Sprague-Dawley rats were injected with streptozotocin to establish experimental diabetic model, then fed without or with 1.2% taurine for additional 4-12 weeks. After that, the protective effects of dietary taurine supplementation on diabetic retinopathy were estimated. Our results showed that chronic taurine supplement effectively improved diabetic retinopathy as changes of histopathology and ultrastructure. The supplementation could not lower plasma glucose concentration (P > 0.05), but caused an elevation in taurine content and a decline in levels of glutamate and gamma-aminobutyric acid (GABA) in diabetic retina (P < 0.05). Moreover, chronic taurine supplementation increased glutamate transporter (GLAST) expression (P < 0.05), decreased intermediate filament glial fibrillary acidic protein (GFAP) and N-methyl-D: -aspartate receptor subunit 1 (NR1) expression in diabetic retina (P < 0.05). These results demonstrated that chronic taurine supplementation ameliorates diabetic retinopathy via anti-excitotoxicity of glutamate in rats.

摘要

本研究的目的是探讨牛磺酸是否能改善糖尿病视网膜病变,并进一步探究其潜在机制。将Sprague-Dawley大鼠注射链脲佐菌素以建立实验性糖尿病模型,然后在无牛磺酸或添加1.2%牛磺酸的情况下再喂养4 - 12周。之后,评估饮食中补充牛磺酸对糖尿病视网膜病变的保护作用。我们的结果表明,长期补充牛磺酸可有效改善糖尿病视网膜病变的组织病理学和超微结构变化。补充牛磺酸不能降低血糖浓度(P>0.05),但可使糖尿病视网膜中的牛磺酸含量升高,谷氨酸和γ-氨基丁酸(GABA)水平降低(P<0.05)。此外,长期补充牛磺酸可增加糖尿病视网膜中谷氨酸转运体(GLAST)的表达(P<0.05),降低中间丝胶质纤维酸性蛋白(GFAP)和N-甲基-D-天冬氨酸受体亚基1(NR1)的表达(P<0.05)。这些结果表明,长期补充牛磺酸可通过抗谷氨酸兴奋性毒性作用改善大鼠糖尿病视网膜病变。

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