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Protective effects of a novel drug RC28-E blocking both VEGF and FGF2 on early diabetic rat retina

International Journal of Ophthalmology(English edition) 2018年第6期11卷 935-944页

作者： Qian-Hui Yang Yan Zhang Jing Jiang Mian-Mian Wu Qian Han Qi-Yu Bo Guang-Wei Yu Yu-Sha Ru Xun Liu Min Huang Ling Wang Xiao-Min Zhang Jian-Min Fang Xiao-Rong Li Tianjin Medical University Eye Hospital Tianjin Medical University Eye Institute College of Optometry and Ophthalmology Tianjin Medical University School of Pharmacy Binzhou Medical University Remegen Ltd. School of Life Sciences and Technology Tongji University

AIM： To investigate protective effects of a novel recombinant decoy receptor drug RC28-E on retinal damage in early diabetic rats. METHODS： The streptozotocin （STZ）-induced diabetic rats were randomly divided into 6 groups： diabetes mellitus （DM） group （saline, 3 μL/eye）; RC28-E at low （0.33 μg/μL, 3 μL）, medium （1 μg/μL, 3 μL）, and high （3 μg/μL, 3 μL） dose groups; vascular endothelial growth factor （VEGF） Trap group （1 μg/μL, 3 μL）; fibroblast growth factor （FGF） Trap group （1 μg/μL, 3 μL）. Normal control group was included. At week 1 and 4 following diabetic induction, the rats were intravitreally injected with the corresponding solutions. At week 6 following the induction, apoptosis in retinal vessels was detected by TUNEL staining. Glial fibrillary acidic protein （GFAP） expression was examined by immunofluorescence. Blood-retinal barrier （BRB） breakdown was assessed by Evans blue assay. Ultrastructural changes in choroidal and retinal vessels were analyzed by transmission electron microscopy （TEM）. Content of VEGF and FGF proteins in retina was measured by enzyme linked immunosorbent assay （ELISA）. The retinal expression of intercellular cell adhesion molecule-1 （ICAM-1）, tumor necrosis factor-α （TNF-α）, VEGF and FGF genes was examined by quantitative polymerase chain reaction （qPCR）. RESULTS： TUNEL staining showed that the aberrantly increased apoptotic cells death in diabetic retinal vascular network was significantly reduced by treatments of medium and high dose RC28-E, VEGF Trap, and FGF Trap （all P〈0.05）, the effects of medium and high dose RC28-E or FGF Trap were greater than VEGF Trap （P〈0.01）. GFAP staining suggested that reactive gliosis was substantially inhibited in all RC28-E and VEGF Trap groups, but the inhibition in FGF Trap group was not as prominent. Evans blue assay demonstrated that only high dose RC28-E could significantly reduce vascular leakage in early diabetic retina （P〈0.01）. TEM revealed that the ultrastructures in choroidal and retinal vessels were damaged in early di

关键词： diabetic retinopathy vascular endothelialgrowth factor fibroblast growth factor 2 recombinant decoy receptor retinal damage diabetes

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Efficacy of granulocyte-colony stimulating factor treatment in a rat model of anterior ischemic optic neuropathy

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Neural Regeneration Research 2014年第16期9卷 1502-1505页

作者： Shun-Ping Huang Rong-Kung Tsai Department of Molecular Biology and Human Genetics Tzu Chi University Institute of Eye Research Buddhist Tzu Chi General Hospital Institute of Medical Sciences Tzu Chi University

Non-arteritic anterior ischemic optic neuropathy （NA-AION） is the most common cause of acute ischemic damage to the optic nerve （ON）, and the leading cause of seriously impaired vision in people over 55 years of age. It demonstrated that subcutaneous administration of Granulocyte colony-stimulating factor （G-CSF） reduces RGC death in an ON crush model in rats, and that the neuroprotective effects may involve both anti-apoptotic and anti-inflammatory processes. Our recent work shows that the protective actions of G-CSF in rAION models may involve both anti-apoptotic and anti-inflammatory processes. However, the exact rescuing mech- anisms involved in the administration of G-CSF in rAION models need further investigation. In addition, further studies on the administration of G-CSF at different time intervals after the induction of rAION may be able to illustrate whether treatment given at a later time is still neu- roprotective. Further, it is unknown whether treatment using G-CSF combined with other drugs will result in a synergistic effect in a rAION model. Inflammation induced by ischemia plays an essential role on the ON head in NA-A1ON, which can result in disc edema and compartment changes. Therefore, it is reasonable that adding an anti-inflammatory drug may enhance the therapeutic effects of G-CSF. An ongoing goal is to evaluate the novel sites of action of both G-CSF and other anti-inflammatory drugs, and to identify the functionally protective pathways to enhance RGC survival. These investigations may open up new therapeutic avenues for the treatment of ischemic optic neuropathy.

关键词： optic nerve anterior ischemic optic neuropathy retinal damage granulocyte colo-ny_stimulating factor inflammatory response

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