| Objectives:It is an important cause that Secondary brain damage after traumatic brain injury (TBI) appeare to lead to brain damage in high mortality.Inflammatory cytokines can be greatly aggravated leading to heavier secondary brain injury. The purpose of this experiment is to investigate the changes of inflammatory factors in brain with TBI in rats by liquid chip technique. And the effect of Taurine(Tau) on the expression of23inflammatory factors, tissue water percentage and GFAP after TBI in rats.To investigate the possible mechanism of the effect of Tau on the expression of inflammatory factors.Methods:A total of96male SD rats were randomly divided into4groups:Sham group,TBI (traumatic brain injury) group,Tau group and Pre-Tau group.Pre-Tau group were administered drugs4days before TBI.Once a day.The latter3groups were performed by lateral fluid percussion.Sham injury was performed by conducting all procedures except the impact injury.The rats were administered drugs(drug dose200mg/kg) intravenously immediately after TBI. Sham groupã€TBI group and Pre-Tau group were given isotonic saline.Once a day.Using liquid chip technology to detect the production of inflammatory factors in the brain samples.24hours and7days after injury,brain was extracted for analysis of cerebral edemaã€cytokine production and the expression of GFAP.The software package SPSS17.0was used for statistical analysis.Results:(1) Compared with Sham group,TBI group caused a significant increase in tissue water percentage at24hours and7days in the penumbra(p<0.05). Compared with TBI group,Tau group and Pre-Tau group obviously decreased tissue water percentage24hours and7days after injury.(2)24h after injury:Compared with Sham group, content of inflammatory factors of TBI groups significant increased(p<0.05),including G-CSFã€Leptinã€MIP-1αã€IL-1βã€IL-6ã€IL-12p70ã€IL-5ã€IL-18ã€MCP-1and RANTES.Compared with TBI group, MIP-1αã€IL-4ã€IL-1βã€IL-12p70ã€IL-18and RANTES obviously decreased in Tau group and G-CSF,Leptin, MIP-1a in Pre-Tau group.(3)7d after injury:Compared with Sham group.content of inflammatory factors of TBI groups significant increased(p<0.05),including G-CSF, Eotaxin, IL-1αã€Leptin〠IL-4ã€IL-1βã€IL-2ã€IL-6ã€IL-13ã€IL-12p70ã€IL-17ã€GRO/KC and TNF-α.Compared with TBI group, G-CSFã€Eotaxinã€IL-1αã€Leptinã€IL4ã€IL-1βã€IL6ã€IL13ã€IL12p70〠IFN-γã€IL-17ã€IP-10ã€VEGFã€TNF-αã€obviously decreased in Tau group.And in Pre-Tau group,MIP-1α,IL-2,RANTES decreased,while the other inflammatory factors are the same as Tau group.(4)Compared with Sham group,TBI group caused a significant increase in the expression of GFAP at7days after injury.Compared with TBI group, the expression of GFAP obviously decreased in Pre-Tau group24hours after injury and in Tau group7days after injury.Conclusions:(1) Taurine can prevent cerebral edema formation in rats after severe TBI whether injected before or after TBI.(2)G-CSFã€Leptinã€MIP-1αã€IL-1βã€IL-6ã€IL-12p70ã€IL-5ã€IL-18ã€MCP-1ã€RANTES are significant increased and Taurine can inhibit the expression of MIP-1αã€IL-4〠IL-1βã€IL-12p70ã€IL-18ã€RANTES in brain24h after TBI. G-CSF, Eotaxin, IL-1α〠Leptinã€IL-4ã€IL-1βã€IL-2ã€IL-6ã€IL-13ã€IL-12p70ã€IL-17ã€GRO/KCã€TNF-a are significant increased and Taurine can inhibit the expression of G-CSFã€Eotaxin〠IL-1αã€Leptin, IL4ã€IL-1βã€IL6ã€IL13ã€IL12p70ã€IFN-γã€IL-17ã€IP-10ã€VEGF〠TNF-α in brain7d after TBI.Taurine may decrease the inflammatory response by inhibiting NF-κB after TBI.(3)Using taurine before TBI Can decrease the expression of GFAP at the early time after TBI.Taurine treatment after TBI can inhibit the expression of GFAP later. Taurine may decrease the inflammatory response by inhibiting the expression of GFAP after TBI... |