Abstract: Objective: To investigate the effect of inhibiting the activation of platelet-derived growth factor receptor α(PDGFRα) on the proliferation of glial cells and the scar formation after brain injury in the mice,and to clarify its mechanism. Methods: A total of 48 8-weeks-old BALB/c mice were selected to establish the damage models of nigra striatum pathway. The model mice were divided into PDGFRα inhibitor AG1296 group(AG1296 group) and DMSO control group (DMSO group) (n=24); the mice in AG1296 group were injected with inhibitor AG1296 along the injured site for 3 d after operation, 5 μ L (5 mmol·L^-1) every day,and the mice in DMSO group were injected with the same dose of DMSO. On the 1st, 4th, 7th and 14th days after operation, 2 mm brain tissues were taken before and after brain injury of every 6 mice were obtained. The expression levels of phosphorylated PDGFRα (p-PDGFRα), glial fibrilary acidic protein(GFAP) and ionized calcium binding adaptor molecle 1(IBA-1) proteins were detected by immunohistochemistry and Western blotting method. The expressions of NG2,CD45,fibronectin (FN) and type Ⅳ collagen (Col Ⅳ) in brain tissue of the mice were detected by immunohistochemistry. Results: The results of immunohistochemistry showed that the number of cells with the brownish yellow positive expression of p-PDGFRα in brain tissue of the mice was the most 4 d after injury,the GFAP perotein had the highest positive expression 14 d after injury,and IBA-1 protein had the highest positive expression 7 d after injury. The expression levels of p-PDGFRα, GFAP,and IBA-1 proteins in brain tissue of the mice in AG1296 group were significantly lower than those in DMSO group at different time points. The results of Western blotting showed that the expression of p-PDGFRα, GFAP and IBA-1 in AG1296 group were significantly lower than those in DMSO control group (P<0.01). The immunohistochemistry staining results showed that the number of NG2,CD45,FN,and ColⅣ positive expression cells in AG1296 group was significantly decreasesd compared with DMSO group 14 d after injury.The scar formation results showed that in AG1296 group, the large cavity in the injury center of brain tissue of the mice disappeared, leaving only a gap; there were still many GFAP positive glial cells around the injury, but there was no obvious boundary membrane, and the number of other positive cells was significantly less than that in DMSO group. Conclusion: Inhibiting the activation of PDGFRα can reduce the proliferation of glial cells after brain injury, and then reduce the formation of scar tissue.

Key words: platelet-derived growth factor receptor, brain injury, astrocytes, microglia, scar