2009PubMedRequires access

[Experimental investigation on protective effect of dexamethasone therapy to traumatic brain injury in rats].

Xiaodong Du, Guoping Li, Lei Ye, Peng Liu, Yu Cao

Open publisher page 2 citations

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.

About this research paper

What this paper is about

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.

Why it matters

OpenAlex reports 2 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available 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.

Key concepts: Dexamethasone, Medicine, Traumatic brain injury, H&E stain, Brain tissue, Immunohistochemistry, Internal medicine, Stain

Related papers

Back to paper searchBrowse research topicsOriginal source
[Experimental investigation on protective effect of dexamethasone therapy to traumatic brain injury in rats]. — Research Paper | ScholarLens