地塞米松治疗与细菌性脑膜炎脑源性神经营养因子及其受体基因表达的关系

目的 探讨地塞米松(DEX)治疗与细菌性脑膜炎脑源性神经营养因子(BDNF)及其受体TrkB基因表达的关系。方法 建立细菌性脑膜炎模型，分别用抗菌药物及抗菌药物加DEX治疗，用原位杂交检测脑组织BDNF mRNA和TrkB mRNA的表达。结果 单独使用抗菌药物治疗后BDNF mRNA和TrkB mRNA表达均低于感染后5d组的水平(P＜0．05)，并以BDNF mRNA下降更明显(P＜0．01)，而使用DEX与抗菌药物联合治疗后，BDNF mRNA和TrkB mRNA表达回到较高水平(P＜0．01)，BDNFmRNA达到感染后5d组水平(P＞0．05)，TrkB mRNA则超过感染后5d组水平(P＜0．05)。结论 DEX则可能通过上调内源性BDNF mRNA和TrkB mRNA表达，有利于抵御细菌性脑膜炎脑损伤。

The relationship between dexamethasone and expression of brain derive neurotrophic factor and its recep tor gene in experimental bacterial meningitis

Objective To investigate the relationship between dexamethasone and brain derive neurotrophic factor gene in experimental bacterial meningitis. Methods To construct the models of bacterial meningitis in 3 weeks old rats(n=33),then 23 of them were administed antibiotic and antibiotic plus dexamethasone respectively. BDNF mRNA and TrkB mRNA in brain was detected by in situ hybridization methods,respectively. Results After administration antibiotics, the expression of BDNF mRNA and TrkB mRNA in brain tissue were less than that in brain after infection 5 d(P< 0.05), especially level of BDNF mRNA was much lower (P< 0.01), and after administration by antibiotics plus DEX, it was greater than that in brain after administration by antibiotics(P< 0.01), the expression of BDNF mRNA was the same as that in brain at 5 d after infection(P> 0.05), the expression of TrkB mRNA was stronger than that in brain at 5 d after infection(P< 0.05). Conclusions The results support the hypothesis that DEX might be propitious to resist brain injury in bacterial menningitis by up-regulation the expression of BDNF mRNA and TrkB mRNA.