Abstract
Abstract: :
Purpose:To study the effect of neuroprotective agent, lithium, on photoreceptor cell degeneration in an experimental model of retinal detachment in mice. Methods: Retinal detachment was induced in the C57BL/6J mice by subretinal injection of 1.4% sodium hyaluronate. Immediately after the surgery, mice were divided into two groups: one group received a diet containing lithium and other received a control diet. At 3, 7, 14, and 28 days after surgery, mice were sacrificed, and retinal sections were collected. Photoreceptor cell survival and apoptosis were assessed by immunohistochemistry and TUNEL. Results: In the control group, photoreceptor cell apoptosis was detected in the detached retina from day 1 after injury, peaked on day 3, and dropped precipitously after day 7. Treatment of lithium abolished photoreceptor cell apoptosis in the first 3 days after retinal detachment. Moreover, it was evident that retinal detachment activated glycogen synthase kinase (GSK)–3ß and other apoptotic signals, while lithium suppressed GSK–3ß activation and increased the expression of anti–apoptotic protein, Bcl–2, in the detached retina. Conclusions: Lithium reduces photoreceptor cell apoptosis associated with retinal detachment by inducing Bcl–2 expression and suppressing the activity of glycogen synthase kinase–3ß in photoreceptor cells. These data suggest that lithium can be used as a potential drug for treating photoreceptor receptor degeneration following retinal detachment.
Keywords: photoreceptors • retinal detachment • apoptosis/cell death