Effects of TF-TP on Human Retinal Pigment Epithelial Cell Damage Induced by Blue Light
Effects of TF-TP on Human Retinal Pigment Epithelial Cell Damage Induced by Blue Light
Lin Li1*, Lu Lu2, Gang An2 and Xiaoguang Zhang3
ABSTRACT
The objective of this study was to investigate the effects of tissue factor targeted peptide (TF-TP) on human retinal pigment epithelial (RPE) cell damage induced by blue light and the potential mechanism. Human RPE cells were divided into blank control group, blue light model group and TF-TP group. The survival rate of human RPE cells and the optimal dose of TF-TP were detected by CCK-8 method. The morphology in the cells were observed under the inverted microscope electron microscope. The apoptosis of the cells was assayed by Hoecht staining. The expressions of TF, Bax and Bcl-2 in the cells were determined by Western blot. After treatment with TF-TP 150 μmol/L, the cell monolayer adhered to the wall, which was fusiform or polygonal. The suspended cells and cell debris were significantly reduced compared with the blue light model group. Hoecht staining showed that the apoptosis rate of the blue light model group and TF-TP 150 μmol/L group was significantly higher than that of the blank control group (P<0.01). The apoptosis rate of TF-TP 150 μmol/L group was significantly lower than that of blue light model group, and the difference was statistically significant (P<0.01). The results of Western Blot assay showed that the TF and Bax proteins in the blue model group were significantly higher than those in the blank control group, and the expression of Bcl-2 protein was significantly decreased (P<0.01). Compared with the blue light model group, the expression of TF and Bax protein in TF-TP 150 μmol/L group was significantly decreased, and the expression of Bcl-2 protein was significantly increased (P<0.01). It was concluded that pretreation of TF-TP could lessen cell apoptosis and increase cell survival rate and therefore plays a protective role to blue light-induced human RPE cells possibly by inhibiting Bax and Bcl-2 pathways mediated by TF.
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