Interleukin-10 improves outcome and alters proinflammatory cytokine expression after experimental traumatic brain injury

摘要: Traumatic injury to the central nervous system initiates inflammatory processes that are implicated in secondary tissue damage. These include synthesis of proinflammatory cytokines, leukocyte extravasation, vasogenic edema, and blood-brain barrier breakdown. Interleukin-10 (IL-10), a cytokine with antiinflammatory properties, negatively modulates cascades at multiple levels. We examined hypothesis IL-10 treatment can improve outcome clinically relevant model traumatic brain (TBI). was administered via different routes dosing schedules lateral fluid-percussion TBI rats. Intravenous administration (100 micrograms) 30 min before 1 h after improved neurological recovery significantly reduced TNF expression traumatized cortex 4 injury. Such associated lower IL-1 injured hippocampus, lesser extent, cortex. Subcutaneous 10 min, 1, 3, 6, 9, 12 also enhanced recovery. In contrast, intracerebroventricular (1 or 6 15 2, 4, 8 not beneficial. results indicate improves suggest this improvement may relate, part, reductions synthesis.