Anti-inflammatory effects of N-cyclooctyl-5-methylthiazol-2-amine hydrobromide on lipopolysaccharide-induced inflammatory response through attenuation of NLRP3 activation in microglial cells
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Microglial activation is closely associated with neuroinflammatorypathologies. The nucleotide-binding and oligomerizationdomain-like receptor containing a pyrin domain 3 (NLRP3) inflammasomesare highly organized intracellular sensors of neuronalalarm signaling. NLRP3 inflammasomes activate nuclearfactor kappa-B (NF-κB) and reactive oxygen species (ROS), whichinduce inflammatory responses. Moreover, NLRP3 dysfunctionis a common feature of chronic inflammatory diseases. The presentstudy investigated the effect of a novel thiazol derivative,N-cyclooctyl-5-methylthiazol-2-amine hydrobromide (KHG26700),on inflammatory responses in lipopolysaccharide (LPS)-treatedBV-2 microglial cells. KHG26700 significantly attenuated theexpression of several pro-inflammatory cytokines, including tumornecrosis factor-α, interleukin-1β, and interleukin-6, in these cells,as well as the LPS-induced increases in NLRP3, NF-κB, andphospho-IkBα levels. KHG26700 also suppressed the LPS-inducedincreases in protein levels of autophagy protein 5 (ATG5), microtubule-associated protein 1 light chain 3 (LC3), and beclin-1,as well as downregulating the LPS-enhanced levels of ROS,lipid peroxidation, and nitric oxide. These results suggest thatthe anti-inflammatory effects of KHG26700 may be due, at leastin part, to the regulation of the NLRP3-mediated signaling pathwayduring microglial activation.
Abstract
Microglial activation is closely associated with neuroinflammatorypathologies. The nucleotide-binding and oligomerizationdomain-like receptor containing a pyrin domain 3 (NLRP3) inflammasomesare highly organized intracellular sensors of neuronalalarm signaling. NLRP3 inflammasomes activate nuclearfactor kappa-B (NF-κB) and reactive oxygen species (ROS), whichinduce inflammatory responses. Moreover, NLRP3 dysfunctionis a common feature of chronic inflammatory diseases. The presentstudy investigated the effect of a novel thiazol derivative,N-cyclooctyl-5-methylthiazol-2-amine hydrobromide (KHG26700),on inflammatory responses in lipopolysaccharide (LPS)-treatedBV-2 microglial cells. KHG26700 significantly attenuated theexpression of several pro-inflammatory cytokines, including tumornecrosis factor-α, interleukin-1β, and interleukin-6, in these cells,as well as the LPS-induced increases in NLRP3, NF-κB, andphospho-IkBα levels. KHG26700 also suppressed the LPS-inducedincreases in protein levels of autophagy protein 5 (ATG5), microtubule-associated protein 1 light chain 3 (LC3), and beclin-1,as well as downregulating the LPS-enhanced levels of ROS,lipid peroxidation, and nitric oxide. These results suggest thatthe anti-inflammatory effects of KHG26700 may be due, at leastin part, to the regulation of the NLRP3-mediated signaling pathwayduring microglial activation.
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