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Intravenous Injection of L-Aspartic Acid β-hydroxamate Attenuates Choroidal Neovascularization via anti-VEGF and Anti-Inflammation

Intravenous Injection of L-Aspartic Acid β-hydroxamate Attenuates Choroidal Neovascularization via anti-VEGF and Anti-Inflammation

Mengjuan Wu, Yimei Liu, He Zhang, Meiling Lian, Juan Chen, Haiyan Jiang, Ying Xu, Ge Shan, Shengzhou Wu

Exp Eye Res. 2019 May;182:93-100.

PMID: 30917905

Abstract:

Choroidal neovascularization (CNV) is a hallmark of exudative age-related macular degeneration (exAMD) and a major cause of visual loss in AMD. Despite the widespread use of anti-VEGF therapy, serious adverse effects arise from repeated intravitreal injection of anti-VEGF antibodies, which warrant alternative strategy. We report herein that in a CNV murine model created by krypton red laser, intravenous injection of a serine racemase inhibitor, l-Aspartic acid β-hydroxamate (L-ABH), significantly reduced CNV at the dose 6 mg/kg on the first day before and followed by 3 mg/kg on the third day after laser injury. The CNV volumes were analyzed with isolectin GS-IB4 staining on choroidal/RPE flat mounts on the seventh day after laser injury. Injection of L-ABH did not produce negative effects on retinal function and visual behavior. To dissect the mechanism in vitro, pretreatment with L-ABH in primary RPE cultures significantly reduced production of vascular endothelial growth factor (VEGF) and macrophage chemotactic protein 1 (MCP-1) by TNFα-primed RPEs. Consistent with these observations, L-ABH pretreatment significantly attenuated macrophage migration mediated by TNFα-primed RPE. Collectively, intravenous injection of L-ABH significantly reduced CNV volumes via reducing production of VEGF and MCP-1 by inflammation-primed RPEs.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP81201981	L-Aspartic acid-4-13C		81201-98-1	Price

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