中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
Celastrol protects mouse retinas from bright light-induced degeneration through inhibition of oxidative stress and inflammation

文献类型:期刊论文

作者Bian, Minjuan2,3; Du, Xiaoye2,3; Cui, Jingang2,3; Wang, Peiwei2,3; Wang, Wenjian2,3; Zhu, Weiliang1; Zhang, Teng2,3; Chen, Yu2,3
刊名JOURNAL OF NEUROINFLAMMATION
出版日期2016-02-27
卷号13
ISSN号1742-2094
DOI10.1186/s12974-016-0516-8
文献子类Article
英文摘要Background: Photoreceptor death leads to vision impairment in several retinal degenerative disorders. Therapies protecting photoreceptor from degeneration remain to be developed. Anti-inflammation, anti-oxidative stress, and neuroprotective effects of celastrol have been demonstrated in a variety of disease models. The current study aimed to investigate the photoreceptor protective effect of celastrol. Methods: Bright light-induced retinal degeneration in BALB/c mice was used, and morphological, functional, and molecular changes of retina were evaluated in the absence and presence of celastrol treatment. Results: Significant morphological and functional protection was observed as a result of celastrol treatment in bright light-exposed BALB/c mice. Celastrol treatment resulted in suppression of cell death in photoreceptor cells, alleviation of oxidative stress in the retinal pigment epithelium and photoreceptors, downregulation of retinal expression of proinflammatory genes, and suppression of microglia activation and gliosis in the retina. Additionally, leukostasis was found to be induced in the retinal vasculature in light-exposed BALB/c mice, which was significantly attenuated by celastrol treatment. In vitro, celastrol attenuated all-trans-retinal-induced oxidative stress in cultured APRE19 cells. Moreover, celastrol treatment significantly suppressed lipopolysaccharides-stimulated expression of proinflammatory genes in both APRE19 and RAW264.7 cells. Conclusions: The results demonstrated for the first time that celastrol prevents against light-induced retinal degeneration through inhibition of retinal oxidative stress and inflammation.
WOS关键词APOPTOSIS IN-VITRO ; 18 KDA TSPO ; MACULAR DEGENERATION ; MICROGLIAL ACTIVATION ; PHOTORECEPTOR DEGENERATION ; NITRIC-OXIDE ; KAPPA-B ; CELLS ; ANTIOXIDANT ; MECHANISMS
资助项目Program of Eastern Scholar at Shanghai Institutions of Higher Learning[00000000] ; Shanghai Municipal Education Commission[13SG42] ; National Natural Science Foundation of China[81473732]
WOS研究方向Immunology ; Neurosciences & Neurology
语种英语
WOS记录号WOS:000370952300001
出版者BIOMED CENTRAL LTD
源URL[http://119.78.100.183/handle/2S10ELR8/276134]  
专题药物发现与设计中心
通讯作者Chen, Yu
作者单位1.Shanghai Inst Mat Med, Shanghai 201203, Peoples R China
2.Shanghai Univ Tradit Chinese Med, Clin Res Inst Integrat Med, Shanghai 200437, Peoples R China;
3.Shanghai Univ Tradit Chinese Med, Yueyang Hosp, 110 Ganhe Rd, Shanghai 200437, Peoples R China;
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GB/T 7714
Bian, Minjuan,Du, Xiaoye,Cui, Jingang,et al. Celastrol protects mouse retinas from bright light-induced degeneration through inhibition of oxidative stress and inflammation[J]. JOURNAL OF NEUROINFLAMMATION,2016,13.
APA Bian, Minjuan.,Du, Xiaoye.,Cui, Jingang.,Wang, Peiwei.,Wang, Wenjian.,...&Chen, Yu.(2016).Celastrol protects mouse retinas from bright light-induced degeneration through inhibition of oxidative stress and inflammation.JOURNAL OF NEUROINFLAMMATION,13.
MLA Bian, Minjuan,et al."Celastrol protects mouse retinas from bright light-induced degeneration through inhibition of oxidative stress and inflammation".JOURNAL OF NEUROINFLAMMATION 13(2016).

入库方式: OAI收割

来源:上海药物研究所

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