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L. Yang, J. Jiao, D. Chen; Lithium Prevents Photoreceptor Cell Apoptosis in Retinal Detachment and Retinitis Pigmentosa Mice. Invest. Ophthalmol. Vis. Sci. 2007;48(13):630.
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To test the neuroprotective effect of lithium on retinal detachment (RD) and retinitis pigmentosa (rd) model of mouse and to understand the mechanism.
Retinal detachment was induced in the C57BL/6J mice followed by feeding with the lithium diet. At 3, 7, 14 and 28 days after surgery, retina sections were collected. FVB/NJ retinal degeneration mice were fed with lithium diet immediately after birth (P0). At day 7 (P7) and day 14 (P14), eyes were removed and retinas were sectioned. Regular diet was treated in both control groups. Histochemistry, TUNEL and immunofluorescent staining were carried out on both the RD and rd mouse retinas to analysis the histology and photoreceptor cell apoptosis.
In lithium-treated retinal detachment mice, the photoreceptor cell apoptosis followed same trend as control. Instead of peaked on day 3 in regular diet mice, the photoreceptor apoptosis peaked on day 7 in lithium-treated mice. Lithium abolished the photoreceptor apoptosis in the first 3 days after the induction of retinal detachment. There is a suppression of GSK-3ß and an increasing of Bcl-2 expression in photoreceptor cells. Meanwhile, in rd mice, the thickness and count of cell layer in P14 was much lower than that in P7 in the control group. But the ONL thickness and count of cell layer was much higher in lithium-treated group than that in the control group in P14. The apoptotic photoreceptor cells were much lower in lithium-treated group than in control.
Lithium abolished photoreceptor apoptosis in both the RD and rd mice. The mechanism of lithium is probably by inhibiting the GSK-3ß and by increasing the expression of Bcl-2 in photoreceptor cells.
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