| Literature DB >> 26629057 |
Xi Yang1, Zhong Shi1, Xia Li1, Jun Li1.
Abstract
The aim of this study was to initially explore the regulatory mechanism of brain function protection of SGB from the view of nerve-endocrine-immune network. 50 patients with traumatic brain injury (TBI) were divided into the SGB treatment group and the control group, the changes of serum IL-6, IL-1β, TNF-α and CGRP levels were detected by ELISA, and the changes of lymphocyte NF-κB protein expression was detected by Western Blot. The control group exhibited the higher expression of IL-6, IL-1β and TNF-α, while the SGB treatment group exhibited various degrees of reduction. On the second day of TBI, the CGRP expression was significantly increased, which was much more significant in the SGB group, and the duration was much longer. The control group exhibited the increased NF-κB p65 and NF-κB p50 after TBI; after the SGB treatment, the NF-κB p65 protein level was significantly reduced, while the NF-κB p50 protein level would not be significantly changed. SGB could chronergically inhibit the excessive inflammatory response in the early post-TBI stage, which suggested that SGB might be involved into the regulation of post-TBI nerve-endocrine-immune system dysfunction.Entities:
Keywords: Traumatic brain injury; calcitonin gene-related peptide; inflammatory cytokine; nerve block; stellate ganglion
Year: 2015 PMID: 26629057 PMCID: PMC4658946
Source DB: PubMed Journal: Int J Clin Exp Med ISSN: 1940-5901