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- Title
A Novel Synthetic Steroid of 2β,3α,5α-Trihydroxy-androst-6-one Alleviates the Loss of Rat Retinal Ganglion Cells Caused by Acute Intraocular Hypertension via Inhibiting the Inflammatory Activation of Microglia.
- Authors
Sun, Hong-Jia-Qi; Xue, Dong-Dong; Lu, Bing-Zheng; Li, Yuan; Sheng, Long-Xiang; Zhu, Zhu; Zhou, Yu-Wei; Zhang, Jing-Xia; Lin, Gan-Jian; Lin, Sui-Zhen; Yan, Guang-Mei; Chen, Yu-Pin; Yin, Wei
- Abstract
Neuroinflammation has been well recognized as a key pathological event in acute glaucoma. The medical therapy of acute glaucoma mainly focuses on lowering intraocular pressure (IOP), while there are still scarce anti-inflammatory agents in the clinical treatment of acute glaucoma. Here we reported that β,3α,5α-trihydroxy-androst-6-one (sterone), a novel synthetic polyhydric steroid, blocked neuroinflammation mediated by microglia/macrophages and alleviated the loss of retinal ganglion cells (RGCs) caused by acute intraocular hypertension (AIH). The results showed that sterone significantly inhibited the morphological changes, the up-regulation of inflammatory biomarker ionized calcium-binding adapter molecule 1 (Iba-1), and the mRNA increase of proinflammatory tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) induced by lipopolysaccharide (LPS) in BV2 microglia and RAW264.7 macrophages. Moreover, immunofluorescence and western blotting analysis revealed that sterone markedly abrogated the nuclear translocation and phosphorylation of nuclear factor-κB (NF-κB) p65 subunit. Furthermore, sterone significantly suppressed the inflammatory microglial activation and RGCs' reduction caused by retinal ischemia/reperfusion (I/R) injury in a rat AIH model. These results suggest sterone may be a potential candidate in the treatment of acute glaucoma caused by microglial activation-mediated neuroinflammatory injury.
- Subjects
INFLAMMATION; RESVERATROL; RETINAL ganglion cells; LABORATORY rats; INTRAOCULAR pressure
- Publication
Molecules, 2019, Vol 24, Issue 2, p252
- ISSN
1420-3049
- Publication type
Article
- DOI
10.3390/molecules24020252