Original Research Article | OPEN ACCESS
Wei-Jiao Zhan,
Jian-Feng Zhu,
Ying Zhang
Department of Ophthalmology, Linyi People’s Hospital, Linyi276000, Shandong, China;
For correspondence:- Ying Zhang
Email: yingzhang487@gmail.com Tel:+865398078282
Received: 1 July 2015
Accepted: 29 December 2015
Published: 28 February 2016
Citation:
Zhan W, Zhu J, Zhang Y.
Retracted: Inhibition of corneal neovascularization by hydrazinocurcumin. Trop J Pharm Res 2016; 15(2):349-354
doi:
10.4314/tjpr.v15i2.18
© 2016 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Abstract
Purpose:To investigate the effect of hydrazinocurcumin on a human vascular endothelial growth factor (VEGF)-induced corneal neovascularization in rabbit model.
Methods: Murine corneal neovascularization (CorNV) was induced via two intrastromal implantations of VEGF polymer 2 mm from the limbus. Hydrazinocurcumin was administered topically on the cornea 4 times daily for 7 days. The therapeutic effects of hydrazinocurcumin were evaluated daily using slit-lamp. At the end of the treatment, the corneas were harvested for H&E staining, masson trichrome staining, immuno-histochemical study, and semi-quantification reverse transcription polymerase chain reaction (RT-PCR) was utilized for measurement of inflammation-related molecules.
Results: Topical application of hydrazinocurcumin had significant therapeutic effects on CorNV Hydrazinocurcumin extract treatment was more effective in suppressing CorNV in terms of vessel length and levels of cluster of differentiation 31 (CD31) proteins or angiogenesis-related genes such as VEGF, matrix metalloproteinase-2 (MMP2) and matrix metalloproteinase-9 (MMP9). The average length of vessels in hydrazinocurcumin-treated group was only 17 % of that in the control group. Hydrazinocurcumin also inhibited inflammation more markedly by more effectively inhibiting mononuclear and polymorphonuclear cell infiltration into the corneal stroma and reducing levels of stromal cell-derived factor-1 (SDF1), tumor necrosis factor-alpha (TNFα) and macrophage inflammatory protein-3 (MIP3a). In addition, the corneas of hydrazinocurcumin group had a more regular and compact architecture of collagen with thinner corneal thickness than those of the untreated group.
Conclusion: Hydrazinocurcumin inhibited human vascular endothelial growth factor (VEGF)-induced rabbit corneal neovascularization and thus can potentially be used for its treatment.
Keywords: Hydrazinocurcumin, Corneal neovascularization, Inflammation, Vascular endothelial growth factor, Corneal thickness