幼年大鼠细菌性脑膜炎脑源性神经营养因子及其mRNA表达的变化

Variation of brain derived neurotrophic factor and its mRNA expression in infancy rats after experimental bacterial meningitis

目的 :探讨细菌性脑膜炎脑源性神经营养因子 (BDNF)及其mRNA的表达特点和所起的作用。方法 :建立 3周龄大鼠细菌性脑膜炎模型和正常对照模型 ,分别于接种后 2 4h、4 8h、5d进行免疫组化染色、原位杂交 ,观察BDNF及其mRNA表达变化。结果 :原位杂交显示感染后 2 4hBDNFmRNA表达明显增加 ,4 8h后有所下降 ,但 5d时仍高于对照组。而免疫组化结果 ,感染后 2 4hBDNF蛋白表达达高峰 ,4 8h后逐渐下降 ,5d时到正常水平。与此同时 ,在软脑膜、蛛网膜下腔、脑室及脑实质炎性病灶内 ,渗出的炎性细胞可见原位杂交阳性信号和免疫组化阳性染色颗粒 ,对照组未见炎性渗出。结论 :细菌性脑膜炎可引起BDNFmRNA和BDNF蛋白表达的增强 ,BDNF可能对细菌性脑膜炎的脑损伤有神经保护作用 ,在急性炎症反应期间 ,可能参与了免疫反应并与其他炎症介质有一定的相关性。

AIM: To investigate the expression and effect of brain derived neurotrophic factor (BDNF) mRNA and its protein in infancy rats after exposure to bacterial meningitis. METHODS: Three week old rats were used to construct the models of bacterial meningitis (n=30) and mormal(n=18). At 24 h, 48 h, 5 d after inoculating, the expression of BDNF mRNA and its protein were detected by in situ hybridization and immunohistochemical staining methods, respectively. RESULTS: The increase in BDNF mRNA expression was detected by in situ hybridization at 24 h in experiment( 0.13320± 0.02750) compared to control( 0.06269± 0.01147)(P<0.01). Expression of BDNF mRNA was declined at 48 h, but its expression was still stronger than that in controls at 5 d(P<0.05). The expression of BDNF protein was enhanced and reached to its zenith at 24 h in this experiment (0.16896±0.02717) (P<0.01), compared to controls(0.08700±0.03413), and it declined after 48 h, then restored to the control levels at 5 d(P>0.05). Meanwhile, in the brain from the experiment rats, strong positive hybridization and immunoreactivity were observed in the infiltrated inflammatory cells in leptomeninges, subarachnoid cavity, ventricles and brain parenchyma. CONCLUSIONS: These results support the hypothesis that BDNF might play a neuroprotective role in brain damage process in bacterial meningitis attacked rats. BDNF might take part in imune response. These results also support the hypothesis that BDNF has some relationships with other inflammatory mediators during acute inflammatory response of bacterial meningitis.