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자료유형
학술저널
저자정보
Eun-A Kim (University of Ulsan College of Medicine) Kyouk Hwang (University of Ulsan College of Medicine) Ji-Eun Kim (Konyang University) Jee-Yin Ahn (Sungkyunkwan University School of Medicine) Soo Young Choi (Hallym University) Seung-Ju Yang (Konyang University) Sung-Woo Cho (University of Ulsan College of Medicine)
저널정보
대한생화학·분자생물학회 BMB Reports BMB Reports 제54권 제11호
발행연도
2021.11
수록면
557 - 562 (6page)

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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.

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