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KW3110 可预防小鼠巨噬细胞炎症应激诱导的线粒体功能障碍。

KW3110 Prevents Inflammatory-Stress-Induced Mitochondrial Dysfunction in Mouse Macrophages.

机构信息

KIRIN Central Research Institute, Kirin Holdings Co., Ltd., Fujisawa 251-8555, Kanagawa, Japan.

出版信息

Int J Mol Sci. 2022 Jan 27;23(3):1443. doi: 10.3390/ijms23031443.

Abstract

KW3110 (KW3110) has anti-inflammatory effects, including the prevention of blue light exposure induced retinal inflammation and ageing-related chronic inflammation in mice. The mechanism involves the promotion of anti-inflammatory cytokine interleukin (IL)-10 production by KW3110, leading to reduced pro-inflammatory cytokine IL-1β production. Although various stress-induced mitochondrial damages are associated with excessive inflammatory responses, the effect of KW3110 on inflammatory-stress-induced mitochondrial damage remains unknown. In this study, we investigated the effect of KW3110 on inflammatory stress-induced mitochondrial damage using the murine macrophage-like cell line J774A.1. KW3110 treatment suppressed lipopolysaccharide (LPS)-induced mitochondrial dysfunction, including downregulation of membrane potential, induction of reactive oxygen species, and respiratory dysfunction. In addition, KW3110 prevented LPS-induced disruption of mitochondrial morphology including cristae structures. IL-10 treatment also ameliorated LPS-induced mitochondrial dysfunction and morphology disruption. These results suggest that KW3110 prevents LPS-induced mitochondrial dysfunction, potentially via promoting IL-10 production in mouse macrophages. We are the first to reveal a suppressive effect of lactic acid bacteria on mitochondrial morphology disruption in inflammatory-stressed macrophages. Our findings contribute to understanding inflammatory-stress-induced mitochondrial damage and developing food ingredients with preventive effects on mitochondrial-damage-derived inflammatory conditions.

摘要

KW3110(KW3110)具有抗炎作用,包括预防蓝光照射诱导的视网膜炎症和小鼠与年龄相关的慢性炎症。其机制涉及 KW3110 促进抗炎细胞因子白细胞介素(IL)-10 的产生,从而减少促炎细胞因子 IL-1β 的产生。尽管各种应激诱导的线粒体损伤与过度炎症反应有关,但 KW3110 对炎症应激诱导的线粒体损伤的影响尚不清楚。在这项研究中,我们使用鼠巨噬细胞样细胞系 J774A.1 研究了 KW3110 对炎症应激诱导的线粒体损伤的影响。 KW3110 处理抑制了脂多糖(LPS)诱导的线粒体功能障碍,包括膜电位下调、活性氧诱导和呼吸功能障碍。此外,KW3110 防止了 LPS 诱导的线粒体形态破坏,包括嵴结构的破坏。IL-10 处理也改善了 LPS 诱导的线粒体功能障碍和形态破坏。这些结果表明,KW3110 通过促进小鼠巨噬细胞中 IL-10 的产生来预防 LPS 诱导的线粒体功能障碍。我们是第一个揭示乳酸菌对炎症应激巨噬细胞中线粒体形态破坏的抑制作用的人。我们的发现有助于理解炎症应激诱导的线粒体损伤,并开发具有预防线粒体损伤引起的炎症状态的食品成分。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af88/8835791/a550333aa762/ijms-23-01443-g001.jpg

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