Liyan Kaiyin Formula relieves reflux pharyngitis by regulating M1 macrophage polarization via the NF-κB/NLRP3 pathway

IF 2.5 4区 医学 Q3 IMMUNOLOGY
Lirong Wang , Xuqing Chen , Tianyu Xu , Youpeng Fei , Qi Yang , Jingjuan An , Zeqing Li , Kunmin Wu
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引用次数: 0

Abstract

Background: We aimed to investigate whether Liyan Kaiyin Formula (LYKYF) can relieve reflux pharyngitis in rats by regulating M1 macrophage polarization via the nuclear factor-κB (NF-κB)/Nod-like receptor protein 3 (NLRP3) pathway.
Methods: Forty rats were randomized into a sham group, a laryngopharyngeal reflux disease (LPRD) group, a LYKYF group and a LYKYF+CHPG group (n = 10). Enzyme-linked immunosorbent assay was conducted to measure the serum levels of inflammatory factors interleukin-6 (IL-6), IL-1β and tumor necrosis factor-α (TNF-α). Western blotting and reverse transcription-polymerase chain reaction (RT-PCR) were performed to measure the expressions of proteins implicated in NF-κB/NLRP3 pathway. Western blotting was also used for the detection of M1 macrophage markers (CD86 and iNOS).
Results: Compared to the sham group, TNF-α, IL-6 and IL-1β levels in the serum, proportion of M1 macrophages in pharyngeal tissues, p-NF-κB p65/p65 ratio, protein expressions of NLRP3, Caspase-1, Apoptosis-associated speck-like protein (ASC), cluster of differentiation 86 (CD86) and inducible nitric oxide synthase, and mRNA expressions of NF-κB p65, NLRP3, Caspase-1 and ASC in the LPRD group exhibited significant elevations (P < 0.05). Compared with the LYKYF group, the LYKYF+CHPG group had significant elevations in serum TNF-α, IL-6 and IL-1β levels, proportion of M1 macrophages in pharyngeal tissues, p-NF-κB p65/p65 ratio, protein expressions of NLRP3, Caspase-1, ASC, CD86 and iNOS, as well as NF-κB p65, NLRP3, Caspase-1 and ASC mRNA expressions (P < 0.05). The identified key target genes were significantly enriched in GO terms associated with signal transduction, protein phosphorylation regulation, and adaptive responses to external stimuli.
Conclusion: LYKYF may suppress M1 macrophage polarization through suppressing the NF-κB/NLRP3 pathway activation, thereby alleviating reflux pharyngitis in rats.
利炎开饮方通过NF-κB/NLRP3通路调节M1巨噬细胞极化,缓解反流性咽炎
背景:我们旨在研究利炎开饮方(LYKYF)是否通过核因子-κB (NF-κB)/ nod样受体蛋白3 (NLRP3)通路调节M1巨噬细胞极化,从而缓解大鼠反流性咽炎。方法:将40只大鼠随机分为假手术组、喉返流病(LPRD)组、LYKYF组和LYKYF+CHPG组(n = 10)。采用酶联免疫吸附法测定血清炎症因子白细胞介素-6 (IL-6)、IL-1β和肿瘤坏死因子-α (TNF-α)水平。采用Western blotting和RT-PCR检测NF-κB/NLRP3通路相关蛋白的表达。Western blotting检测M1巨噬细胞标志物(CD86和iNOS)。结果:与假手术组比较,LPRD组大鼠血清TNF-α、IL-6、IL-1β水平、咽部组织M1巨噬细胞比例、P -NF-κB p65/p65比值、NLRP3、Caspase-1、凋亡相关斑点样蛋白(ASC)、CD86、诱导型一氧化氮合酶蛋白表达、NF-κB p65、NLRP3、Caspase-1、ASC mRNA表达均显著升高(P <;0.05)。与LYKYF组比较,LYKYF+CHPG组血清TNF-α、IL-6、IL-1β水平、咽部组织M1巨噬细胞比例、P -NF-κB p65/p65比值、NLRP3、Caspase-1、ASC、CD86、iNOS蛋白表达以及NF-κB p65、NLRP3、Caspase-1、ASC mRNA表达均显著升高(P <;0.05)。鉴定出的关键靶基因显著富集与信号转导、蛋白磷酸化调控和对外部刺激的适应性反应相关的氧化石墨烯。结论:LYKYF可能通过抑制NF-κB/NLRP3通路激活来抑制M1巨噬细胞极化,从而减轻大鼠反流性咽炎。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Immunobiology
Immunobiology 医学-免疫学
CiteScore
5.00
自引率
3.60%
发文量
108
审稿时长
55 days
期刊介绍: Immunobiology is a peer-reviewed journal that publishes highly innovative research approaches for a wide range of immunological subjects, including • Innate Immunity, • Adaptive Immunity, • Complement Biology, • Macrophage and Dendritic Cell Biology, • Parasite Immunology, • Tumour Immunology, • Clinical Immunology, • Immunogenetics, • Immunotherapy and • Immunopathology of infectious, allergic and autoimmune disease.
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