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Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành hóa học dành cho các bạn yêu hóa học tham khảo đề tài: Lateral fluid percussion injury of the brain induces CCL20 inflammatory chemokine expression in rats | Das et al. Journal of Neuroinflammation 2011 8 148 http www.jneuroinflammation.eom content 8 1 148 JJOURNAL1 OF. NEUROINFLAMMATION RESEARCH Open Access Lateral fluid percussion injury of the brain induces CCL20 inflammatory chemokine expression in rats Mahasweta Das1 Christopher C Leonardo2 Saniya Rangooni1 Shyam S Mohapatra1 4 Subhra Mohapatra3 4 and Keith R Pennypacker2 Abstract Background Traumatic brain injury TBI evokes a systemic immune response including leukocyte migration into the brain and release of pro-inflammatory cytokines however the mechanisms underlying TBI pathogenesis and protection are poorly understood. Due to the high incidence of head trauma in the sports field battlefield and automobile accidents identification of the molecular signals involved in TBI progression is critical for the development of novel therapeutics. Methods In this report we used a rat lateral fluid percussion impact LFPI model of TBI to characterize neurodegeneration apoptosis and alterations in pro-inflammatory mediators at two time points within the secondary injury phase. Brain histopathology was evaluated by fluoro-jade FJ staining and terminal deoxynucleotidyl transferase dUTP nick end labelling TUNEL assay polymerase chain reaction qRT PCR enzyme linked immunosorbent assay ELISA and immunohistochemistry were employed to evaluate the CCL20 gene expression in different tissues. Results Histological analysis of neurodegeneration by FJ staining showed mild injury in the cerebral cortex hippocampus and thalamus. TUNEL staining confirmed the presence of apoptotic cells and CD11b microglia indicated initiation of an inflammatory reaction leading to secondary damage in these areas. Analysis of spleen mRNA by PCR microarray of an inflammation panel led to the identification of CCL20 as an important pro-inflammatory signal upregulated 24 h after TBI. Although CCL20 expression was observed in spleen and thymus after 24h of TBI it was not expressed in degenerating cortex or .
