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Anti-inflammatory effects of N-cyclooctyl-5-methylthiazol-2-amine hydrobromide on lipopolysaccharide-induced inflammatory response through attenuation of NLRP3 activation in microglial cells
Eun-A Kim1 (Research worker), Kyouk Hwang1 (College student), Ji-Eun Kim2 (Graduate student), Jee-Yin Ahn3 (Professor), Soo Young Choi4 (Professor), Seung-Ju Yang2 (Professor), Sung-Woo Cho1,* (Professor)
1Biochemistry and Molecular Biology, University of Ulsan College of Medicine,
2Biomedical Laboratory Science, Konyang University,
3Molecular Cell Biology and Single Cell Network Research Center, Sungkyunkwan University School of Medicine,
4Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University
Abstract
Microglial activation is closely associated with neuroinflammatory pathologies. The nucleotide-binding and oligomerization domain-like receptor containing a pyrin domain 3 (NLRP3) inflammasomes are highly organized intracellular sensors of neuronal alarm signaling. NLRP3 inflammasomes activate nuclear factor kappa-B (NF-リB) and reactive oxygen species (ROS), which induce inflammatory responses. Moreover, NLRP3 dysfunction is a common feature of chronic inflammatory diseases. The present study investigated the effect of a novel thiazol derivative, N-cyclooctyl-5-methylthiazol-2-amine hydrobromide (KHG26700), on inflammatory responses in lipopolysaccharide (LPS)-treated BV-2 microglial cells. KHG26700 significantly attenuated the expression of several pro-inflammatory cytokines, including tumor necrosis factor-メ, interleukin-1モ, and interleukin-6, in these cells, as well as the LPS-induced increases in NLRP3, NF-リB, and phospho-IkBメ levels. KHG26700 also suppressed the LPS-induced increases 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 that the anti-inflammatory effects of KHG26700 may be due, at least in part, to the regulation of the NLRP3-mediated signaling pathway during microglial activation.
Abstract, Accepted Manuscript(in press) [Submitted on June 28, 2021, Accepted on July 22, 2021]
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