作者: Nicoletta Charolidi , Tom Schilling , Claudia Eder
DOI: 10.1371/JOURNAL.PONE.0128463
关键词: Brain damage 、 Stimulation 、 Immunology 、 Chemokine 、 Endocrinology 、 Biology 、 Microglia 、 Proinflammatory cytokine 、 Neuroinflammation 、 CXCL1 、 Cytokine 、 Internal medicine
摘要: Brain tissue damage following stroke or traumatic brain injury is accompanied by neuroinflammatory processes, while microglia play a central role in causing and regulating neuroinflammation via production of proinflammatory substances, including cytokines chemokines. Here, we used slices, an established situ model, from young adult aged mice to investigate cytokine chemokine with particular focus on the microglia. Twenty four hours after slice preparation, higher concentrations cytokines, i.e. TNF-α IL-6, chemokines, CCL2 CXCL1, were released slices than mice. However, maximal microglial stimulation LPS for 24 h did not reveal age-dependent differences amounts Mechanisms underlying appear be similar Inhibition Kv1.3 channels margatoxin reduced release but CXCL1. In contrast, blockade P2Y12 receptors PSB0739 inhibited whereas IL-6 remained unaffected. Cytokine was inhibitors Kir2.1 K+ adenosine receptors. summary, our data suggest that damage-induced chemokines age-dependent, differentially regulated