Barichello Tatiana, Silva Geruza Z, Savi Geovana D, Torquato Joana M, Batista Ana L, Scaini Giselli, Rezin Gislaine T, Santos Patricia M, Feier Gustavo, Streck Emilio L
Laboratório de Fisiopatologia Experimental, Programa de Pós-Graduação em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Criciúma, SC, Brazil.
Brain Res Bull. 2009 Aug 28;80(1-2):85-8. doi: 10.1016/j.brainresbull.2009.04.011. Epub 2009 May 4.
Bacterial meningitis due to Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae including sensory-motor deficits, seizures, and impairments of learning and memory. Creatine kinase (CK) is an effective buffering system of cellular ATP levels in high-energy consuming tissues; a decrease in CK activity is associated with a neurodegenerative pathway that results in neuronal loss. Thus, the aim of this study was to evaluate brain CK activity after pneumococcal meningitis. The animals underwent a magna cistern tap receiving either sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension; they were killed 6, 12, 24 and 48h after that, the brain was removed and hippocampus, striatum, cerebellum, cerebral cortex and prefrontal cortex were dissected and used for the determination of CK activity. We verified that CK activity was not altered 6 and 12h after meningitis. Interestingly, 24h after the induction of the meningitis we observed a decrease in CK activity. Finally, CK activity was not altered 48h after meningitis. Although it is difficult to extrapolate our findings to the human condition, the inhibition of brain CK activity may be involved in the pathogenesis of pneumococcal meningitis.
由肺炎链球菌引起的细菌性脑膜炎与显著的死亡率以及持续的神经后遗症相关，这些后遗症包括感觉运动缺陷、癫痫发作以及学习和记忆障碍。肌酸激酶（CK）是高能量消耗组织中细胞ATP水平的有效缓冲系统；CK活性降低与导致神经元丧失的神经退行性途径相关。因此，本研究的目的是评估肺炎球菌脑膜炎后脑CK活性。动物接受大池穿刺，分别注射无菌生理盐水作为安慰剂或等量的肺炎链球菌悬液；之后在6、12、24和48小时将它们处死，取出大脑，解剖海马体、纹状体、小脑、大脑皮层和前额叶皮层，用于测定CK活性。我们证实脑膜炎后6小时和12小时CK活性未改变。有趣的是，在诱发脑膜炎24小时后，我们观察到CK活性降低。最后，脑膜炎后48小时CK活性未改变。尽管很难将我们的研究结果外推至人类情况，但脑CK活性的抑制可能参与了肺炎球菌脑膜炎的发病机制。
