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Title: Immediate splenectomy decreases mortality and improves cognitive function of rats after severe traumatic brain injury
Authors: Li, M
Li, F
Luo, C
Shan, Y
Zhang, L
Qian, Z
Zhu, G
Lin, J
Feng, H
Keywords: Brain edema
Cognitive function
Traumatic brain injury
Issue Date: 2011
Publisher: Lippincott Williams & Wilkins
Source: Journal of trauma - injury, infection and critical care, 2011, v. 71, no. 1, p. 141-147 How to cite?
Journal: Journal of Trauma - Injury, Infection and Critical Care 
Abstract: BACKGROUND: Traumatic brain injury (TBI) is a major health problem all over the world. It frequently causes a considerable social burden because of its high incidence of death and long-term disability, especially in the case of severe TBI. Recent studies revealed that the spleen might contribute to secondary brain injury after ischemia or intracerebral hemorrhage. The purpose of this study was to evaluate the significance of the spleen in traumatic brain edema after severe TBI. METHODS: We established a severe TBI model with rats and performed splenectomy to observe the mortality, brain water content, cognitive function (water maze), and cytokines levels, including interleukin (IL)-1β, tumor necrosis factor-α (TNF-α), IL-6, and IL-10, in the blood plasma (enzyme-linked immunosorbent assay) and their mRNA expression levels in injured brain tissue (quantitative reverse transcriptase-polymerase chain reaction). RESULTS: The immediate splenectomy after TBI significantly decreased the death rate from 35.42% to 14.89% and eliminated the brain water content of the injured brain, especially at days 2 and 3. The Morris water maze assessment showed an improved spatial reference memory in rats that underwent both TBI and splenectomy when compared with those in the TBI group, 4 weeks later. Splenectomy reduced the IL-1β, TNF-α, and IL-6 contents in the blood serum after TBI, and the mRNA expression levels of IL-1β, TNF-α, and IL-6 in the ipsilateral brain tissue also decreased. CONCLUSIONS: Our study demonstrates that splenectomy has a protective effect on rats with severe TBI by inhibiting proinflammatory cytokines, including IL-1β, TNF-α, and IL-6, both systematically and locally in the injured brain, hence leading to a decreased mortality and improved cognitive function.
DOI: 10.1097/TA.0b013e3181f30fc9
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