2 Subconjunctival fibrosis and scar formation is a major cause of surgical failure. In trabeculectomy, the gold standard glaucoma surgery, the postoperative wound healing response is the main determinant of resistance to aqueous egress and, therefore, surgical success. It suggests a potential therapeutic strategy worth further exploration with a view towards postoperative wound healing modulation in glaucoma filtration surgery. This in vitro study focused on investigations of irbesartan's effects on HTF migration, ROS production, as well as HTF cell numbers and morphology. This initial study warrants future investigations for further potential antifibrotic effects of this drug. Angiotensin II increased cell number without altering morphology.
It also reduced cell numbers and altered HTF morphology. Irbesartan inhibited HTF migration and ROS production. Conversely, angiotensin II increased cell numbers up to 4-fold while retaining cell viability. Irbesartan reduced cell numbers by 50% and induced morphologic changes with loss of pseudopods ( P < 0.05). Levels of ROS were almost completely attenuated by irbesartan (DHE fluorescence intensity of 5.68E-09) ( P < 0.05). Irbesartan inhibited HTF migration by 50% to 70% compared to controls ( P < 0.05). To assess the effect on reactive oxygen species (ROS) level, HTF were treated with either irbesartan (10 μg/mL) or angiotensin II (2 μg/mL) for 24 hours after scratching, and then stained with dihydroethidium (DHE) before evaluation by confocal microscopy. The extent of HTF migration up to 30 hours, and cell number and morphology at 72 hours was evaluated. We investigate the effect of angiotensin receptor blockade on the migration of human Tenon fibroblasts (HTF), using irbesartan, an angiotensin II receptor type 1 (AT1R) blocker (ARB) as a potential antifibrotic agent in glaucoma filtration surgery.Ĭonfluent HTF cultures were scratched with a 1 mL pipette tip and treated with either irbesartan (10, 50, and 100 μg/mL) or angiotensin II (2 μg/mL).
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