Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 1 de 1
Filter
Add filters








Language
Year range
1.
Chinese Journal of Applied Clinical Pediatrics ; (24): 1404-1406, 2014.
Article in Chinese | WPRIM | ID: wpr-453788

ABSTRACT

Objective To investigate the dynamic level changes and significance of triggering receptor expressed on myeloid cells-1 (TREM-1) in the injury brain tissues of rats caused by pneumolysin (PLY).Methods Sixty-four SD rats were randomly and equally divided into PLY group and control group,0.1 mL PLY and isopyknic normal saline was given through left internal carotid artery respectively.Brain tissue gross and histological changes were observed at different time(4 h,6 h,12 h,24 h),meanwhile the expression levels of neurocyte damage marker glial fibrillary acidic protein (GFAP) and neuron-specific enolase (NSE) protein were detected by immunohistochemistry;and the expression levels of TREM-1,tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected respectively by enzyme-linked immunosorbent assay.Results The observation of brain tissue gross and histological changes indicated the existence of brain injury,and the expression levels of GFAP,NSE,TNF-α and IL-6 protein increased from 4 h after PLY were injected and augmented dynamically as time went on,compared with the control group at corresponding time points,the differences were statistically significant (all P < 0.05).The level of TREM-1 in the PLY group reached a peak at the 4 h time point,but decreased somewhat at the 6 h time point,the level of TREM-1 was still higher than that in control group,the differences were statistically significant(all P < 0.05).However,the level of TREM-1 in the PLY group declined obviously at 12 h and 24 h time points,compared with that in control group,there were no significant differences (all P > 0.05).Conclusions The expression levels of TREM-1 up-regulated obviously in the early stage of brain damage induced by PLY,which might be involved in the pathological process of brain damage by promoting the expression of TNF-α and IL-6.

SELECTION OF CITATIONS
SEARCH DETAIL