Abstract
Microglial hyperactivation and neuroinflammation are known to induce neuronal death, which is one of the main causes of neurodegenerative disorders. We previously found that Aquilariae Lignum extract attenuated both neuronal excitotoxicity and neuroinflammation in vivo and in vitro. For further analysis, we extracted the methylene chloride fraction of Aquilariae Lignum to determine the bioactive compounds. In this study, we investigated the anti-neuroinflammatory effects and underlying mechanisms of the Aquilariae Lignum fraction (ALF) using lipopolysaccharide (LPS)-stimulated BV2 microglial cells. BV2 cells were pretreated with ALF (0.5, 1, and 2.5 μg/mL) before treatment with LPS (1 μg/mL). Pretreatment with ALF significantly attenuated the LPS-induced overproductions of nitric oxide (NO), cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and interleukin (IL)-1β. These anti-inflammatory effects were supported by ALF-mediated modulation of the nuclear factor-kappa B (NF-κB) pathway. Furthermore, ALF exerted strong anti-inflammasome effects, as shown by IL-1β-specific inhibitory activity, but not activity against tumor necrosis factor (TNF)-α, along with inhibition of caspase-1 activity and NACHT, LRR, and PYD domain-containing protein 3 (NLRP3)-related molecules. These results indicate the potent anti-neuroinflammatory activity of ALF and that its underlying mechanism may involve the regulation of NLRP3 inflammasome-derived neuroinflammation in microglial cells.
Highlights
The inflammatory response is an immune defense mechanism to cope with harmful environmental conditions [1]
The reactive microglial phenotype can lead to neuronal damage via excessive release of inflammatory cytokines, such as tumor necrosis factor (TNF)-α or interleukin (IL)-1β [3,4]
Excessive release of inflammatory vascular remodeling of the blood–brain barrier (BBB), which eventually leads to neuronal death could alter the vascular remodeling of the blood–brain barrier (BBB), which eventually leads to
Summary
The inflammatory response is an immune defense mechanism to cope with harmful environmental conditions [1]. Various mechanisms are known to contribute to neuroinflammation, the NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome pathway is emerging as an. LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome pathway is emerging as an important pathologic process [7]. VX-765 doseinduces synaptic loss, neuronal apoptosis, and even mouse structural remodeling in the hippocampus dependently reversed cognitive impairment and neuropathology [11]. NLRP3 inflammasome pathway is considered a therapeutic strategy for neurodegenerative diseases cognitive impairment and neuropathology [11]. East Asianand regions previously that Aquilariae has the Lignum has the potential to inhibit microglial overactivation in the mouse hippocampus [15]. Thein above suggest the involvement of microglia-derived neuroinflammation as a neuroinflammation as a target mechanism of Lignum. During the process of identifying target mechanism of Aquilariae Lignum.
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