中文摘要：

目的通过观察自发性高血压大鼠（SHR）脑白质损伤的病理改变和检测炎症相关指标，探讨炎症反应在SHR脑白质损伤中的作用。方法选择18只40周龄雄性SHR为实验组，同龄7只雄性Wistar-Kyoto（WKY）大鼠为对照组，取动物脑组织，应用HE染色及免疫组织化学染色，观察其病理改变及胶质酸性蛋白、神经中丝、髓鞘碱性蛋白的含量改变。同时取大鼠脑白质组织，使用荧光实时定量PCR技术，检测Toll样受体4（TLR-4）和单核细胞趋化蛋白1（MCP-1）以及与血管细胞黏附分子1（VCAM-1）的mRNA表达水平。结果40周龄SHR脑白质出现明显损伤。HE染色显示出现脑白质疏松，免疫染色显示白质区星形胶质细胞活化、神经轴索数量减少以及脱髓鞘改变。相对于WKY，SHR脑白质TLR-4、MCP-1和VCAM-1的mRNA表达明显增高，差异有统计学意义（P〈0．05）；相对于脑白质损伤程度较轻的SHR，程度较重的SHR中TLR-4、MCP-1和VCAM-1 mRNA表达水平更高，差异有统计学意义（P〈0．05）。结论SHR脑白质损伤情况与脑白质疏松症类似；炎症反应参与脑白质损伤的病理生理过程，是导致脑白质损伤的因素之一。

英文摘要：

Objective To study the role of inflammation in white matter damage of spontaneously hypertensive rats （SHRs） through observing the pathology changes of tissues after white matter damage and detecting the levels of inflammation-related indicators. Methods Eighteen 40-week-old male SHRs were chosen as experimental group, and seven male Wistar-Kyoto （WKY） rats were used as control group. The animal brain tissues were taken for hematoxylin-eosin staining （HE staining） and immunohistochemical staining to observe the pathological changes, and the levels of myelin basic protein （MBP）, neurofilament （NF） and glial fibrillary acidic protein （GFAP）. Real-time PCR was employed to detect toll-like receptor 4 （TLR-4）, monocyte chemotactic protein 1 （MCP-1） and vascular cell adhesion molecule-1 （VCAM-1） expression levels in the white matter tissues. Results The white matter of 40-week-old SHRs was apparently injured. HE staining displayed sponge-like changes in the white matter and immunohistochemical staining showed astrocyte activation, reduced number of axonal and demyelination in the white matter. As compared with those in the WKY rats, TLR-4, MCP-1 and VCAM-1 mRNA expressions in SHR white matter were significantly increased （P〈0.05）; and TLR-4, MCP-1 and VCAM-1 expression levels in SHRs were positively related to the degree of white matter damage. Conclusion The white matter damage in 40-week-old SHRs is similar to that of LA; inflammation is involved in the pathophysiological process of white matter damage, being one of inducedfactors of white matter injury.