Muranaka Kimimasa, Yanagi Yasuo, Tamaki Yasuhiro, Takahashi Hidenori, Usui Tomohiko, Ohashi Koji, Matsuoka Hidehito, Senda Toshihiko
Department of Ophthalmology, University of Tokyo School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan.
FEBS Lett. 2005 Nov 7;579(27):6084-8. doi: 10.1016/j.febslet.2005.09.079. Epub 2005 Oct 7.
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.
研究了一种合成环状二硫化物化合物SA3443对血管生成的影响。在体外，酶联免疫吸附测定和逆转录聚合酶链反应表明，SA3443在蛋白质和mRNA水平上均抑制了ARPE - 19细胞中缺氧诱导的血管内皮生长因子（VEGF）的表达。在体内，给激光诱导脉络膜新生血管（CNV）的小鼠施用SA3443可抑制病变部位的渗漏并减小其大小。此外，施用SA3443可显著降低VEGF蛋白的表达水平。综上所述，我们的结果表明，SA3443可抑制VEGF的产生，并减少血管渗漏和小鼠实验性CNV的生长。
