[Experimental investigation on protective effect of dexamethasone therapy to traumatic brain injury in rats].
Xiaodong Du, Guoping Li, Lei Ye, Peng Liu, Yu Cao
Abstract
Xiaodong Du, Guoping Li, Lei Ye, Peng Liu, Yu Cao
Abstract
OBJECTIVE: To explore the effects of dexamethasone on nuclear factor-KappaB (NF-KappaB) expression in brain tissue after traumatic brain injury (TBI). METHODS: Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-KappaB in brain tissue of rats was detected by immunohistochemical method. RESULTS: NF-KappaB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0.01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0.05 or P<0.01). After treatment with dexamethasone, NF-KappaB level was lowered at 6, 24 and 72 hours (all P<0.01). CONCLUSION: NF-KappaB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-KappaB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.
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OBJECTIVE: To explore the effects of dexamethasone on nuclear factor-KappaB (NF-KappaB) expression in brain tissue after traumatic brain injury (TBI). METHODS: Forty rats were randomly divided into two groups: dexamethasone treatment and no treatment, and severe brain injury was produced by gas percussion in both groups. At 0, 6, 24, 72 and 120 hours after injury, 5 rats of each group were executed and the histopathological changes in brain tissue in rats were observed by hematoxylin-eosin (HE) stain. The expression of NF-KappaB in brain tissue of rats was detected by immunohistochemical method. RESULTS: NF-KappaB expression was significantly up-regulated at 6 hours in brain tissue of rats after TBI (P<0.05), reaching the highest level at 24 hours (P<0.01). It showed a tendency to lower, but was still high at 120 hours after TBI (P<0.05 or P<0.01). After treatment with dexamethasone, NF-KappaB level was lowered at 6, 24 and 72 hours (all P<0.01). CONCLUSION: NF-KappaB expression is up-regulated in brain tissue in early period after TBI, and keeps on a high level, thus inducing inflammatory response to produce secondary injury to brain tissue. Dexamethasone shows protective effects by regulating the levels of NF-KappaB and prevents secondary injury which is caused by the inflammatory cytokines in rat brain tissue after TBI.
Key concepts: Dexamethasone, Medicine, Traumatic brain injury, H&E stain, Brain tissue, Immunohistochemistry, Internal medicine, Stain