Laboratório de Microbiologia Experimental, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 888806-000, Criciúma, SC, Brasil Center for Experimental Models in Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Medical School at Houston, 77030, Houston, TX, USA
Laboratório de Microbiologia Experimental, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, 888806-000, Criciúma, SC, Brasil.
Exp Biol Med (Maywood). 2014 Oct;239(10):1360-5. doi: 10.1177/1535370214535896. Epub 2014 Jun 5.
Streptococcus pneumoniae is the relevant cause of bacterial meningitis, with a high-mortality rate and long-term neurological sequelae, affecting up to 50% of survivors. Pneumococcal compounds are pro-inflammatory mediators that induce an innate immune response and tryptophan degradation through the kynurenine pathway. Vitamin B6 acts as a cofactor at the active sites of enzymes that catalyze a great number of reactions involved in the metabolism of tryptophan, preventing the accumulation of neurotoxic intermediates. In the present study, we evaluated the effects of vitamin B6 on memory and on brain-derived neurotrophic factor (BDNF) expression in the brain of adult Wistar rats subjected to pneumococcal meningitis. The animals received either 10 µL of artificial cerebral spinal fluid (CSF) or an equivalent volume of S. pneumoniae suspension. The animals were divided into four groups: control, control treated with vitamin B6, meningitis, and meningitis treated with vitamin B6. Ten days after induction, the animals were subjected to behavioral tests: open-field task and step-down inhibitory avoidance task. In the open-field task, there was a significant reduction in both crossing and rearing in the control group, control/B6 group, and meningitis/B6 group compared with the training session, demonstrating habituation memory. However, the meningitis group showed no difference in motor and exploratory activity between training and test sessions, demonstrating memory impairment. In the step-down inhibitory avoidance task, there was a difference between training and test sessions in the control group, control/B6 group, and meningitis/B6 group, demonstrating aversive memory. In the meningitis group, there was no difference between training and test sessions, demonstrating impairment of aversive memory. In the hippocampus, BDNF expression decreased in the meningitis group when compared to the control group; however, adjuvant treatment with vitamin B6 increased BDNF expression in the meningitis group. Thus, vitamin B6 attenuated the memory impairment in animals subjected to pneumococcal meningitis.
肺炎链球菌是细菌性脑膜炎的相关病因，具有高死亡率和长期神经后遗症，影响多达 50%的幸存者。肺炎球菌化合物是促炎介质，通过犬尿氨酸途径诱导先天免疫反应和色氨酸降解。维生素 B6 作为在催化色氨酸代谢中涉及的大量反应的酶的活性部位的辅助因子起作用，防止神经毒性中间产物的积累。在本研究中，我们评估了维生素 B6 对接受肺炎球菌性脑膜炎的成年 Wistar 大鼠的记忆和大脑源性神经营养因子 (BDNF) 表达的影响。动物接受 10 μL 人工脑脊液 (CSF) 或等量的肺炎球菌混悬液。动物分为四组：对照组、对照组用维生素 B6 处理、脑膜炎组和脑膜炎用维生素 B6 处理。诱导后 10 天，动物进行行为测试：旷场任务和下台阶抑制回避任务。在旷场任务中，与训练阶段相比，对照组、对照/B6 组和脑膜炎/B6 组的穿越和竖起次数均显著减少，表明习惯记忆。然而，脑膜炎组在训练和测试阶段之间的运动和探索活动没有差异，表明记忆受损。在下台阶抑制回避任务中，对照组、对照/B6 组和脑膜炎/B6 组在训练和测试阶段之间存在差异，表明厌恶记忆。在脑膜炎组中，在训练和测试阶段之间没有差异，表明厌恶记忆受损。在海马体中，与对照组相比，脑膜炎组的 BDNF 表达降低；然而，辅助用维生素 B6 增加了脑膜炎组的 BDNF 表达。因此，维生素 B6 减轻了接受肺炎球菌性脑膜炎的动物的记忆障碍。
