期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 373, 期 4, 页码 504-508出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.06.069
关键词
ischemia; cobalt chloride (CoCl2); gap junctions; retinal degeneration; hypoxia; caspase-3; HIF1-alpha; PQ1
资金
- NEI NIH HHS [R01 EY013421-07, R03 EY015670-03, R01 EY013421-06S1] Funding Source: Medline
- NIA NIH HHS [R01 AG025500, R01AG025500] Funding Source: Medline
- PHS HHS [EYR0113421] Funding Source: Medline
Retinal cells which become ischemic will pass apoptotic signal to adjacent cells, resulting in the spread of damage. This occurs through open gap junctions. A class of novel drugs, based on primaquine (PQ), was tested for binding to connexin 43 using simulated docking studies. A novel drug has been synthesized and tested for inhibition of gap junction activity using R28 neuro-retinal cells in culture. Four drugs were initially compared to mefloquine, a known gap junction inhibitor. The drug with optimal inhibitory activity, PQ1, was tested for inhibition and was found to inhibit dye transfer by 70% at 10 mu M. Retinal ischemia was produced in R28 cells using cobalt chloride as a chemical agent. This resulted in activation of caspase-3 which was prevented by PQ1, the gap junction inhibitor. Results demonstrate that novel gap junction inhibitors may provide a means to prevent retinal damage during ischemia. (C) 2008 Elsevier Inc. All rights reserved.
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