摘要
目的探讨钠-钾-氯共转运体1(Na+-K+-2Cl-cotransporter 1,NKCC1)抑制剂布美他尼处理(BT)对小鼠创伤性脑损伤(TBI)早期的脑保护作用及可能分子信号调控机制。方法成年雄性BALB/c小鼠54只,随机分为对照组,颅脑创伤组(TBI组)和布美他尼治疗组(BTT组)各18只,采用Mamarou加速性颅脑损伤方法制备小鼠TBI模型。采用HE染色法观察各组小鼠皮层损伤程度;利用神经功能学评分(NSS)进行神经功能学评分;干湿重法检测脑组织含水量;同时,Western blot法检测磷酸化细胞外调节蛋白激酶(p-ERK)、细胞外调节蛋白激酶(ERK)蛋白的表达变化。结果与TBI组比较,BTT组皮层神经元损伤减轻,同时,BTT组小鼠神经功能学评分优于TBI组(P<0.05);TBI后12 h,BTT组p-ERK的蛋白表达水平低于TBI组(P<0.01)。结论抑制NKCC1的表达可能发挥重要的脑保护作用,而p-ERK可能参与NKCC1的信号调控机制。
Objective To investigate the protective mechanism of Burmetanide (BT, an inhibitor of Na+-K+- 2Cl-cotransporter 1 ) on traumatic brain injury (TBI) mouse model. Methods Fifty-four BALB/c mice were randomly divided into three groups, control group, TBI group, BT treatment group (BIT group) with 18 in each group. The Mamarou TBI model was used in TBI and BTF groups. HE staining method we used to observe the damage of neuron cells in the cortical area. The neurological severity score (NSS) and wet-dry weighing method were used to observe the injury of mice. The expressions of phosphorylated extracelltdar regulated protein kinases (p- ERK) and extracellular regulated protein kinases (ERK) were examined by Western blot. Results There was less water content in the BIT group compared with TBI group. The severity of neurons damage in the BTT group was less than that in TBI group. The expression of p-ERK of HIT group was lower than that of TBI group (P 〈 0. 05). Conclusion BT may play a vital role in the TBI at early stage by inhibiting the expression of p-ERK.
出处
《中华神经外科疾病研究杂志》
CAS
2012年第6期495-498,共4页
Chinese Journal of Neurosurgical Disease Research
基金
国家自然科学基金资助项目(30930093
81200949)
十二五国家科技支撑计划基金资助项目(2012BAI11B02)
陕西省科技计划基金资助项目(2012JQ4005)
西京医院学科助推计划基金资助项目(XJZT12T05)