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Abstract
Objectives: Inflammation is involved in the occurrence and progression of Parkinson’s disease (PD), but the exact mechanisms remain unclear. This study aimed to observe the expressions of glial fibrillary acidic protein (GFAP) and integrin αM (CD11b) in the substantia nigra and striatum, and to investigate the effect of eldepryl on these expressions in a rat model of PD.
Methods: Seventy-two rats were randomly divided into three groups: control, model, and eldepryl. Each group was randomly divided into 4-day and 8-day subgroups (n = 12 rats/group) after successful establishment of the model. The rat model of PD was established by subcutaneous injection of rotenone through the back of the neck. After model establishment, the rats were given physiological saline in the control and model groups, and eldepryl in the eldepryl group for 4 or 8 days. The numbers of GFAP-positive and CD11b-positive cells and expressions of GFAP and CD11b were detected by immunohistochemistry and western blotting analysis, respectively.
Results: GFAP-positive and CD11b-positive cells changed from their normal quiescent state into a so-called reactive state. GFAP and CD11b expressions were upregulated in the substantia nigra and striatum in the model group compared with the control group (p < 0.05), but there were no significant differences between 8 and 4 days (p > 0.05). In the eldepryl group, GFAP and CD11b expressions were decreased compared with the model group (p < 0.05), with a significant decrease for 8 days compared with 4 days (p < 0.05).
Discussion: Glial cells were greatly proliferated and activated in the substantia nigra and striatum of rats with PD, and eldepryl could prevent the progression of PD by inhibiting the proliferation and activation of glial cells.