Suppression of laser‐induced choroidal neovascularization by oral administration of SA3443 in mice

Abstract

The effect of a synthetic cyclic disulfide compound, SA3443, on neovascularization was investigated. In vitro, enzyme-linked immunosorbent assay and RT-PCR demonstrated that SA3443 suppressed the expression of the hypoxia-induced vascular endothelial growth factor (VEGF) at both protein and mRNA levels in ARPE-19 cells. In vivo, the administration of SA3443 to mice with laser-induced choroidal neovascularization (CNV) suppressed the leakage from the lesions and reduced their size. Furthermore, the expression level of VEGF protein was significantly reduced by the administration of SA3443. Taken together, our results demonstrate that SA3443 suppresses VEGF production and reduces vascular leakage and the growth of mouse experimental CNV.

Bone morphogenetic protein‐4 enhances vascular endothelial growth factor secretion by human retinal pigment epithelial cells

“…ARPE-19 cells have also been shown to release vascular endothelial growth factor (VEGF) in response to amino acid deprivation (metabolic stress; [Abcouwer et al, 2002]), 4-hydroxynonenal (oxidative stress; [Ayalasomayajula and Kompella, 2002]), and SA3443, a synthetic cyclic disulfide compound (anti-inflammation; [Muranaka et al, 2005]). Pfeffer et al [1994] showed that human RPE cells produce transforming growth factor-beta 2 (TGF-β2) and Pascal et al [1999] showed that TGF-β2 production can be affected by different glucose concentrations.…”

Aster koraiensis Extract and Chlorogenic Acid Inhibit Retinal Angiogenesis in a Mouse Model of Oxygen‐Induced Retinopathy

“…Vascular endothelial growth factor (VEGF) is a well-known proangiogenic and vascular permeability factor, and is a key mediator in the pathogenesis of these retinal diseases [ 3 ]. Recently, the use of VEGF antagonists to inhibit the VEGF signaling pathway has successfully diminished retinal neovascularization in several experimental animal models [ 4 ] and human subjects [ 5 ]. In numerous clinical trials, intravitreally injected anti-VEGF agents, including bevacizumab, ranibizumab, and aflibercept, notably suppressed neovascularization and stabilized vision loss [ 6 – 8 ].…”

EGHB010, a Standardized Extract of Paeoniae Radix and Glycyrrhizae Radix, Inhibits VEGF‐Induced Tube Formation In Vitro and Retinal Vascular Leakage and Choroidal Neovascularization In Vivo

“…Vascular endothelial growth factor (VEGF) is a well-known proangiogenic and vascular permeability factor and a key mediator in the pathogenesis of wet AMD and diabetic retinopathy [ 4 , 5 ]. Recently, the use of VEGF antagonists to inhibit VEGF signaling pathway has successfully diminished the formation of CNV in several experimental animal models [ 6 ] and human subjects [ 7 ]. In numerous clinical trials, intravitreally injected anti-VEGF agents, such as bevacizumab, ranibizumab, and aflibercept, notably suppressed neovascularization and stabilized vision loss in patients with neovascular AMD [ 8 – 10 ] and improved retinal edema and vision in patients with diabetic macular edema [ 11 ].…”