Cellular inflammatory response associated with breakdown of the blood-brain barrier after closed head injury in rats.

摘要: This study reports a widespread microglial response characterized by an upregulation of surface antigens, such as complement type 3 receptors (CR3) and major histocompatibility complex (MHC) class II antigens on these cells following closed head injury. Increased expression CR3 (OX-42) MHC (OX-6) was observed in rats killed at 1, 3, 5 days after Intense OX-42 immunoreactivity throughout the brain with smaller number them being OX-6 positive. In addition to reaction, astrocytic activation reflected cellular hypertrophy increased for glial fibrillary acidic protein (GFAP) Together above, diffuse perivascular intraneuronal immunostaining immunoglobulin G (IgG) primarily cerebral cortex. accompanied enhanced both endothelial nitric oxide synthase (eNOS) blood vessels inducible (iNOS) macrophages. subjected injury followed single intraperitoneal (i.p.) injection rhodamine isothiocyanate (RhIc), seepage fluorescent dye into neuropil observed. had resulted labelling cortical neurons clearly demonstrating breakdown blood-brain barrier (BBB). latter, it is conceivable that ensuing leakage plasma immunoglobulins other serum-derived materials could induce microglia. The mechanism causing BBB dysfunction not clear, although present results suggest excessive release (NO) may be contributory factor. microglia suggests their involvement endocytosis immunological responses.