Protective effect of Shengfu injection on rats with acute traumatic brain injury

Wang Lu; Luo Ke; Qing Guo-zhong; Zhou Jia; Lu Yu; Peng Zheng-liang; Yin Jian; Huang Kai-liang

doi:10.3969/j.issn.1002-1949.2017.11.017

Abstract：Objective To investigate the effects of Shenfu injection on expression level of glutamate transporter (GLT-1) and GLAST signaling pathway,the early serum S100β protein,total calcium and water content in brain tissue of rats with acute traumatic brain injury.Methods Sixty male SD mice,weighing 300 ～ 320 g,were equally and randomly divided into 3 groups(n =20 each) using a random number table:sham group (group Sham),acute traumatic brain injury group (group ATBI),andshengfu injection group (group SF).Models of ATBI were made according to Feeney's methods.Shengfu injection 20 mL/kg preconditioning was injected intraperitoneally 30 min before making the model in group SF,while the equal volume of normal saline was given in Sham and ATBI groups.The serum S100β protein was measured at 15 min (T1) and 60 min (T2) after modeling.The rats were sacrificed 4 h after modeling and the total calcium and water content were measured.GLT-1 and GLAST mRNA were detected by RT-PCR,The expression of GLT-1 and GLAST protein was detected by Western blot.Results Compared with T1,the content of S100β protein of T2 in ATBI and SF groups was significantly decreased (P ＜ 0.05).Compared with Sham group,the content of S100β protein,the total calcium and water content of brain tissue in ATBI and SF groups were significantly increased,and the expression of GLT-1,GLAST mRNA and GLT-1 and GLAST protein in brain tissue were significantly decreased (P ＜ 0.05).Compared with ATBI group,the contents of serum S100β protein,total calcium and water content in brain tissue were significantly decreased,and the expression of GLT-1,GLAST mRNA and GLT-1 and GLAST protein in brain tissue were significantly increased(P ＜ 0.05).Conclusion Shenfu injection can relieve acute traumatic brain injury in rats,and its mechanism may be related with its up-regulation of glutamate transporter activity and GLAST signaling pathway.