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Microglial Activation Modulates Neuroendocrine Secretion During Experimental Sepsis
Molecular Neurobiology ( IF 4.6 ) Pub Date : 2021-01-07 , DOI: 10.1007/s12035-020-02241-5
Luis Henrique Angenendt da Costa 1 , Nilton Nascimento Santos-Junior 1 , Carlos Henrique Rocha Catalão 1 , Maria José Alves Rocha 1, 2, 3
Affiliation  

Sepsis promotes an inflammatory state in the central nervous system (CNS) that may cause autonomic, cognitive, and endocrine changes. Microglia, a resident immune cell of the CNS, is activated in several brain regions during sepsis, suggesting its participation in the central alterations observed in this disease. In this study, we aimed to investigate the role of microglial activation in the neuroendocrine system functions during systemic inflammation. Wistar rats received an intracerebroventricular injection of the microglial activation inhibitor minocycline (100 μg/animal), shortly before sepsis induction by cecal ligation and puncture. At 6 and 24 h after surgery, hormonal parameters, central and peripheral inflammation, and markers of apoptosis and synaptic function in the hypothalamus were analyzed. The administration of minocycline decreased the production of inflammatory mediators and the expression of cell death markers, especially in the late phase of sepsis (24 h). With respect to the endocrine parameters, microglial inhibition caused a decrease in oxytocin and an increase in corticosterone and vasopressin plasma levels in the early phase of sepsis (6 h), while in the late phase, we observed decreased oxytocin and increased ACTH and corticosterone levels compared to septic animals that did not receive minocycline. Prolactin levels were not affected by minocycline administration. The results indicate that microglial activation differentially modulates the secretion of several hormones and that this process is associated with inflammatory mediators produced both centrally and peripherally.



中文翻译:

小胶质细胞激活调节实验性脓毒症期间的神经内分泌分泌

脓毒症促进中枢神经系统 (CNS) 的炎症状态,可能导致自主神经、认知和内分泌变化。小胶质细胞是 CNS 的一种常驻免疫细胞,在脓毒症期间在几个大脑区域被激活,表明它参与了在这种疾病中观察到的中枢改变。在这项研究中,我们旨在研究小胶质细胞激活在全身炎症期间神经内分泌系统功能中的作用。在通过盲肠结扎和穿刺诱导脓毒症前不久,Wistar 大鼠接受了小胶质细胞激活抑制剂米诺环素(100 μg/动物)的脑室内注射。在手术后 6 和 24 小时,分析了下丘脑的激素参数、中枢和外周炎症以及细胞凋亡和突触功能的标志物。米诺环素的给药减少了炎症介质的产生和细胞死亡标志物的表达,尤其是在脓毒症晚期(24 小时)。在内分泌参数方面,在脓毒症早期(6 小时),小胶质细胞抑制导致催产素降低,皮质酮和加压素血浆水平升高,而在晚期,我们观察到催产素降低,ACTH 和皮质酮水平升高与未接受米诺环素的败血症动物相比。催乳素水平不受米诺环素给药的影响。结果表明,小胶质细胞激活对几种激素的分泌有不同的调节,并且该过程与中枢和外周产生的炎症介质有关。

更新日期:2021-01-07
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