Abstract
Objective To investigate the transformation of the brain edema and the expression of endothelin-1 (ET-1) mRNA in brain following diffuse brain injury (DBI) in order to study the mechanism of magnesium sulfate for DBI.Methods Eighty male SD rats were randomly divided into three groups:control (n =5),DBI (they was divided into ten subgroups,n =5),and treatment group (they was divided into five subgroups,n =5).Diffuse contusion and laceration of brain was produced by Marmarou' s brain injury model.The water cotained in brain and the expression of ET-1 mRNA at different time points after DBI were determined.The expression of ET-1 mRNA was detected by using real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR) in two groups.The water contained in the brain after pure brain injury and treatment was determined.Results The expression of ET-1 mRNA was upregnlated rapidly after DBI,reached the peak at 6th h,then declined slowly.Karskal-wallis test revealed that there was significant difference in the expression of ET-1 mRNA among groups,P ＜0.01.The water contained in damaged brain was increased rapidly at 6th h.Kurskal-wallis test showed that the water contained in damaged brain was different among groups,and reached higher level at 12th h.The expression of ET-1 mRNA in treatment group was lower than in pure brain injury group at the same time point between two groups by t test.The water contained in the brain of treatment group was decreased as compared with that in the control group at the same time point.Conclusion (1) The expression of ET-1 mRNA following DBI is upregulated rapidly in a short time,and reaches the top at 6th h; (2) The water contained in damaged brain is increased rapidly,and reaches higher level at 12th h; (3) The expression of ET-1 mRNA following DBI can upregulate the water contained in the damaged brain.The water contained in the brain following DBI is dechned after injection of magnesium sulfate by micropump probably by reducing the expression of ET-1 mRNA,resulting in the decreased ET-1 synthesis,and alleviating the ischemia-hypoxia of the brain and its toxicity to the brain. Key words: Diffuse brain injury; Endothelin-1 ; Brain edema
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