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解淀粉芽孢杆菌通过减轻泡沫细胞形成和巨噬细胞极化来防治动脉粥样硬化。

Bacillus amyloliquefaciens Protect Against Atherosclerosis Through Alleviating Foam Cell Formation and Macrophage Polarization.

机构信息

Department of Cardiology, Zhejiang Provincial People's Hospital, No. 158 Shangtang Road, Hangzhou, 310014, Zhejiang, China.

出版信息

Curr Microbiol. 2024 Jul 13;81(9):263. doi: 10.1007/s00284-024-03775-w.

Abstract

This study was to investigate the therapeutic effect of Bacillus amyloliquefaciens (Ba) on atherosclerosis (AS). THP-1 monocyte was differentiated to THP-1 macrophage (THP-M) through phorbol 12-myristate 13-acetate. After pre-treatment by 10 cfu/ml Ba lasting 6 h, THP-M was induced with 100 mg/l ox-LDL lasting 48 h to form macrophage foam cell (THP-F). RT-qPCR and flow cytometry were employed to determine the polarization of THP-M and THP-F. ApoE mice with high-fat and high-cholesterol diet were used for constructing an AS model to evaluate the effect of Ba on AS. Our in vitro results showed that Ba vegetative cells pre-treatment distinctly inhibited the levels of iNOS and CD16/CD32 (M1 macrophage markers), and increased the levels of FIZZ1, Ym1, Arg1, CD163, and CD206 (M2 macrophage markers), indicating that Ba pre-treatment promoted anti-inflammatory M2-like polarization both in THP-M and THP-F. Meanwhile, it also suppressed cholesterol uptake, esterification, and hydrolysis, and efflux by THP-M and THP-F. Additionally, our animal experiments demonstrated that Ba vegetative cells treatment suppressed high cholesterol, hyperglycemia, hyperlipidemia, and the release of inflammatory factors (TNF-α, IL-6 and IL-1β) in ApoE AS mice. In a word, our results indicated that Ba may protect against AS through alleviating foam cell formation and macrophage polarization through targeting certain stages of AS.

摘要

本研究旨在探讨解淀粉芽胞杆菌(Ba)对动脉粥样硬化(AS)的治疗作用。通过佛波醇 12-肉豆蔻酸 13-乙酸酯将 THP-1 单核细胞分化为 THP-1 巨噬细胞(THP-M)。用 10 cfu/ml Ba 预处理 6 h 后,用 100 mg/l 氧化低密度脂蛋白(ox-LDL)诱导 THP-M 48 h 形成巨噬细胞泡沫细胞(THP-F)。采用 RT-qPCR 和流式细胞术检测 THP-M 和 THP-F 的极化情况。采用高脂高胆固醇饮食构建载脂蛋白 E(ApoE)小鼠 AS 模型,评价 Ba 对 AS 的作用。我们的体外结果显示,Ba 营养细胞预处理可明显抑制 iNOS 和 CD16/CD32(M1 巨噬细胞标志物)的水平,增加 FIZZ1、Ym1、Arg1、CD163 和 CD206(M2 巨噬细胞标志物)的水平,表明 Ba 预处理可促进 THP-M 和 THP-F 的抗炎 M2 样极化。同时,还抑制了 THP-M 和 THP-F 的胆固醇摄取、酯化和水解以及外排。此外,动物实验表明,Ba 营养细胞治疗可抑制 ApoE AS 小鼠的高胆固醇、高血糖、高血脂和炎症因子(TNF-α、IL-6 和 IL-1β)的释放。总之,我们的研究结果表明,Ba 可能通过减轻泡沫细胞形成和巨噬细胞极化来防治 AS,其作用靶点可能涉及 AS 的某些阶段。

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