Glibenclamide Prevents Inflammation by Targeting NLRP3 Inflammasome Activation in vitro

IF 0.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Evolutionary Biochemistry and Physiology Pub Date : 2024-06-26 DOI:10.1134/s002209302403013x
E. D. Khilazheva, Yu. A. Panina, A. I. Mosiagina, O. S. Belozor, Yu. K. Komleva
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Abstract

The NLRP3 inflammasome plays a significant role in the development of neurodegeneration, physiological aging and metabolic inflammation, which actualizes the search for effective NLRP3 inflammasome inhibitors and assessing their effects. This study was aimed to assess the effect of pharmacological modulation of NLRP3 activity by an indirect NLRP3 inflammasome inhibitor, glibenclamide, on the in vitro expression of metaflammasome components in brain cells derived from middle-aged mice. It was found that glibenclamide reduces the expression of pro-inflammatory markers NLRP3 and IL18 in cell culture, which in turn prevents the phosphorylation of metaflammasome complex protein kinases, PKR and IKKβ. At the same time, there were no changes in the expression of pathologically phosphorylated IRS, as well as in the number of senescent cells in cultures after glibenclamide exposure.

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格列本脲通过靶向激活 NLRP3 炎症小体预防体外炎症
摘要 NLRP3炎症小体在神经退行性病变、生理衰老和代谢性炎症的发生发展中起着重要作用,这就需要寻找有效的NLRP3炎症小体抑制剂并评估其作用。本研究旨在评估间接NLRP3炎症小体抑制剂格列本脲通过药物调节NLRP3活性对中年小鼠脑细胞中元炎症小体成分体外表达的影响。研究发现,格列本脲能降低细胞培养中促炎症标志物NLRP3和IL18的表达,进而阻止元飞沫体复合蛋白激酶、PKR和IKKβ的磷酸化。同时,格列本脲暴露后,病理磷酸化 IRS 的表达以及培养物中衰老细胞的数量均无变化。
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来源期刊
自引率
33.30%
发文量
110
审稿时长
6-12 weeks
期刊介绍: Journal of Evolutionary Biochemistry and Physiology  publishes original experimental and theoretical and review articles related to evolution of the main forms of metabolism in connection with life origin; comparative and ontogenetic physiology and biochemistry, biochemical evolution of animal world; as well as evolution of functions; morphology, pharmacology, pathophysiology and ecological physiology. The journal welcomes manuscripts from all countries in the English or Russian language.
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