ABSTRACT
Objective To investigate the influence of Ethyl pyruvate(EP) on the level of high mobility group box 1 (HMGB1) in brain injury of infant rats induced by lipopolysaccharide (LPS) and its significance.Methods Two hundred and forty normal healthy 1-month-old Spragne-Dawley (SD) rats were randomly divided into 3 groups:9 g/L sodium chloride (NS) group(n=80),LPS group (n=80),and EP group (n=80).LPS (1 mg/kg) was injected via internal carotid.In EP group,after injecting LPS,each rat was immediately administrated 4 mL EP(40 mg/kg) intraperitoneally; in control group,4 mL Ringer's solution was given instead of EP.Rats were decapitated at 6,12,24,48 and 72 h following drug injection.The evan's blue (EB) content of brain tissues was meteraged by the formamide methods.Immunohistochemistry technology was used to detect the expression of HMGB1,neuron specific enolase(NSE) and glial fibrillary acidic protein(GFAP) protein,and reverse transcribe polymerase chain reaction technology was applied to study the expression level of HMGB1 mRNA in brain tissue.Meanwhile,the pathological changes of brain tissues were observed under the light microscope.Results Six hours after LPS was given,brain EB content,the levels of NSE,GFAP protein started to rise,reaching the peak at 24 h,and still higher than those in control group at 48 h and 72 h.The expression pattern of HMGB1 protein and mRNA in brain tissue was consistent with the severity of brain injury,increased at 6 h after LPS was given and reached the peak at 24 h,still higher than those in control group at 48 h and 72 h.Positive correlation was found among HMGB1 protein,HMGB1 mRNA and EB content,NSE protein,GFAP protein,respectively.In EP group,the levels of HMGB1 protein and mRNA,the levels of brain EB content,NSE,GFAP protein were found,positive correlation was still gotten between HMGB1 protein,EB content and NSE,GFAP protein,HMGB1 mRNA in LPS group and EP group.Conclusion EP has neuroprotective effect on brain injury induced by LPS,which may be relevant to decreasing of the expression of HMGB1 and suppressing inflammation action.