Liu Bin, Lv Chaonan, Zhang Jinxia, Liu Ying, Sun Jing, Cheng Xiaohua, Mao Wenjing, Ma Yuanyuan, Li Shiying
a First Department of Neurology , Hospital Affiliated to North China University of Science and Technology , Tangshan , China.
Neurol Res. 2017 May;39(5):459-467. doi: 10.1080/01616412.2017.1297911. Epub 2017 Mar 9.
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.
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.
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).
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.
炎症参与帕金森病（PD）的发生和发展，但其确切机制仍不清楚。本研究旨在观察黑质和纹状体中胶质纤维酸性蛋白（GFAP）和整合素αM（CD11b）的表达，并探讨司来吉兰对PD大鼠模型中这些表达的影响。
72只大鼠随机分为三组：对照组、模型组和司来吉兰组。模型成功建立后，每组再随机分为4天和8天亚组（每组n = 12只大鼠）。通过颈后皮下注射鱼藤酮建立PD大鼠模型。模型建立后，对照组和模型组大鼠给予生理盐水，司来吉兰组给予司来吉兰，持续4天或8天。分别通过免疫组织化学和蛋白质印迹分析检测GFAP阳性和CD11b阳性细胞的数量以及GFAP和CD11b的表达。
GFAP阳性和CD11b阳性细胞从正常的静止状态转变为所谓的反应性状态。与对照组相比，模型组黑质和纹状体中GFAP和CD11b的表达上调（p < 0.05），但8天和4天之间无显著差异（p > 0.05）。与模型组相比，司来吉兰组GFAP和CD11b的表达降低（p < 0.05），8天与4天相比有显著降低（p < 0.05）。
PD大鼠的黑质和纹状体中胶质细胞大量增殖和激活，司来吉兰可通过抑制胶质细胞的增殖和激活来阻止PD的进展。
