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首页> 外文期刊>Journal of neurotrauma >Ceftriaxone treatment after traumatic brain injury restores expression of the glutamate transporter, GLT-1, reduces regional gliosis, and reduces post-traumatic seizures in the rat
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Ceftriaxone treatment after traumatic brain injury restores expression of the glutamate transporter, GLT-1, reduces regional gliosis, and reduces post-traumatic seizures in the rat

机译：颅脑外伤后头孢曲松的治疗可恢复谷氨酸转运蛋白GLT-1的表达，减少区域性胶质增生，并减少大鼠的创伤后癫痫发作

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Excessive extracellular glutamate after traumatic brain injury (TBI) contributes to excitotoxic cell death and likely to post-traumatic epilepsy. Glutamate transport is the only known mechanism of extracellular glutamate clearance, and glutamate transporter 1 (GLT-1) is the major glutamate transporter of the mammalian brain. We tested, by immunoblot, in the rat lateral fluid percussion injury TBI model whether GLT-1 expression is depressed in the cortex after TBI, and whether GLT-1 expression after TBI is restored after treatment with ceftriaxone, a well-tolerated β-lactam antibiotic previously shown to enhance GLT-1 expression in noninjured animals. We then tested whether treatment with ceftriaxone mitigates the associated regional astrogliosis, as reflected by glial fibrillary acid protein (GFAP) expression, and also whether ceftriaxone treatment mitigates the severity of post-traumatic epilepsy. We found that 7 days after TBI, GLT-1 expression in the ipsilesional cortex was reduced by 29% (n=7/group; p<0.01), relative to the contralesional cortex. However, the loss of GLT-1 expression was reversed by treatment with ceftriaxone (200 mg/kg, daily, intraperitoneally). We found that ceftriaxone treatment also decreased the level of regional GFAP expression by 43% in the lesioned cortex, relative to control treatment with saline (n=7 per group; p<0.05), and, 12 weeks after injury, reduced cumulative post-traumatic seizure duration (n=6 rats in the ceftriaxone treatment group and n=5 rats in the saline control group; p<0.001). We cautiously conclude that our data suggest a potential role for ceftriaxone in treatment of epileptogenic TBI.
机译：脑外伤（TBI）后过量的细胞外谷氨酸导致兴奋性毒性细胞死亡，并可能导致创伤后癫痫。谷氨酸转运是细胞外谷氨酸清除的唯一已知机制，而谷氨酸转运蛋白1（GLT-1）是哺乳动物脑中主要的谷氨酸转运蛋白。我们通过免疫印迹测试了大鼠侧脑液per打损伤TBI模型在TBI后皮质中GLT-1表达是否降低，以及在用耐受良好的β-内酰胺头孢曲松治疗后TBI后GLT-1表达是否恢复先前显示的抗生素可增强非受伤动物的GLT-1表达。然后，我们测试了头孢曲松治疗是否能减轻神经胶质纤维酸性蛋白（GFAP）的表达，从而减轻相关的区域性星形胶质增生，还测试头孢曲松治疗是否能减轻创伤后癫痫的严重程度。我们发现，在TBI后7天，同病灶皮层相比，同病灶皮层中GLT-1的表达降低了29％（n = 7 /组; p <0.01）。但是，头孢曲松（200 mg / kg，每天，腹膜内）治疗可逆转GLT-1表达的丧失。我们发现，相对于生理盐水的对照治疗（每组n = 7; p <0.05），头孢曲松钠治疗还使病变皮层中的区域GFAP表达水平降低了43％，并且在受伤后12周降低了术后累积累积外伤性癫痫发作持续时间（头孢曲松治疗组n = 6只大鼠和生理盐水对照组n = 5只; p <0.001）。我们谨慎地得出结论，我们的数据表明头孢曲松钠在治疗癫痫性TBI中具有潜在作用。

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