Regulation of microglial activation in stroke

Abstract

When ischemic stroke occurs, oxygen and energy depletion triggers a cascade of events, including inflammatory responses, glutamate excitotoxicity, oxidative stress, and apoptosis that result in a profound brain injury. The inflammatory response contributes to secondary neuronal damage, which exerts a substantial impact on both acute ischemic injury and the chronic recovery of the brain function. Microglia are the resident immune cells in the brain that constantly monitor brain microenvironment under normal conditions. Once ischemia occurs, microglia are activated to produce both detrimental and neuroprotective mediators, and the balance of the two counteracting mediators determines the fate of injured neurons. The activation of microglia is defined as either classic (M1) or alternative (M2): M1 microglia secrete pro-inflammatory cytokines (TNFα, IL-23, IL-1β, IL-12, etc) and exacerbate neuronal injury, whereas the M2 phenotype promotes anti-inflammatory responses that are reparative. It has important translational value to regulate M1/M2 microglial activation to minimize the detrimental effects and/or maximize the protective role. Here, we discuss various regulators of microglia/macrophage activation and the interaction between microglia and neurons in the context of ischemic stroke.

Self-assembly of 2-aldehyde-8-hydroxyquinolinate-based lanthanide complexes and NIR luminescence

“…885.1 eV and 902.8 eV binding energy of Ce 3d 5/2 and Ce 3d 3/2 , respectively, which are in agreement with the reported values[24]. S and S 0 peaks at 898.0 and 916.0 eV stand for the characteristic satellite signals of Ce 4+ ions.X-ray crystallographic analysis reveals that 3-5 are isomorphous in the triclinic space group PÀ1, and they possess similar host structure as 2.…”

Acute exposure to diesel exhaust impairs adult neurogenesis in mice: prominence in males and protective effect of pioglitazone

“…It should be noted that microglia may either promote or inhibit adult neurogenesis (Sato 2015), depending on the activation state (Aarum et al 2003; Xu et al 2017). Notably, the M2 activation state, which is induced by anti-inflammatory cytokines such as IL-4, favors proliferation, and can direct neural progenitor cells (NPC) towards neurogenesis (Cherry et al 2014; Choi et al 2017; Zhao et al 2017). In contrast, the inflammatory cytokines such as interferon-γ and TNFα, as well as oxidative stress, induce the M1 (classical activation) state, provoking killing behavior in microglia and other macrophages (Colton 2009).…”

The Role of Alpha-Lipoic Acid in the Pathomechanism of Acute Ischemic Stroke

“…As shown in Fig. 2, no neurological deficits [17,18]), however the Garcia scores in the control (8 [7,10]), LA20 (10 [8, 12]) and LA40 groups (13 [10,15]) were significantly lower (P < 0.05). Additionally, rats treated with 20 and 40 mg/kg of α-LA showed greatly improved neurological behavior compared with rats in the control group (P < 0.05).…”