Inflammatory mechanism of white matter damage in spontaneously hypertensive rats
10.3760/cma.j.issn.1671-8925.2013.01.006
- VernacularTitle:自发性高血压大鼠的脑白质损伤及其炎症反应机制
- Author:
Pei CHEN
1
;
Chuan-Qiang QU
;
Chuan-Zhu YAN
;
Hong-Zhi GUO
;
Cui-Lan WANG
Author Information
1. 山东大学齐鲁医院脑血管病科
- Keywords:
Spontaneously hypertension;
Leukoaraiosis;
Toll-like receptor 4;
Monocyte chemotactic protein 1;
Vascular cell adhesion molecule-1
- From:
Chinese Journal of Neuromedicine
2013;12(1):24-28
- CountryChina
- Language:Chinese
-
Abstract:
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 induced factors of white matter injury.
