良血祛湿止阳汤通过fc γ r介导的吞噬作用抑制小鼠特应性皮炎。

IF 4.4 3区 医学 Q2 CELL BIOLOGY
Mediators of Inflammation Pub Date : 2025-04-27 eCollection Date: 2025-01-01 DOI:10.1155/mi/7068964
Lili Zhang, Linxian Li, Zhanxue Sun
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引用次数: 0

摘要

背景:良血祛湿止阳汤是治疗特应性皮炎(AD)的传统方剂。然而,LQZ减轻AD症状的具体机制在很大程度上仍然未知。本研究的目的是探讨LQZ对AD的保护作用,并揭示其潜在的作用机制。方法:用2,4-二硝基氯苯(DNCB)建立小鼠AD模型。小鼠口服LQZ或强的松龙(PDN)。在整个治疗期间,定期监测小鼠的皮炎评分和抓挠频率。采用苏木精伊红(H&E)染色和甲苯胺蓝(TB)染色进行组织病理学分析。采用酶联免疫吸附法(ELISA)检测血清炎症因子水平。进一步,采用串联质量标签(TMT)标记定量蛋白质组学方法鉴定差异表达蛋白(DEPs)。富集分析确定了LQZ治疗作用的潜在靶点和通路。最后,通过验证实验进一步探索LQZ治疗AD的具体途径和核心靶点。结果:清芪可明显减轻DNCB诱导的AD小鼠皮肤屏障损伤和炎症反应,降低血清IgE、IL-4、IL-1β水平。蛋白质组学分析鉴定出248个差异表达蛋白,暗示LQZ的治疗作用涉及多种途径。其中,FcγR (FcγR)介导的吞噬途径成为AD炎症和免疫反应的关键因素。与该途径相关的关键蛋白,包括Fc-gamma RIII (Fcgr3)、v -ye -1山口肉瘤病毒相关癌基因同源物(Lyn)、酪氨酸蛋白激酶(Syk)、磷酸肌苷磷脂酶C-gamma-2 (Plcg2)、中性粒细胞胞质因子1 (Ncf1)、ras相关C3肉毒毒素底物2 (Rac2)和肌动蛋白相关蛋白2/3复合物亚基3 (Arpc3),在LQZ治疗后表达水平显著降低。结论:泻泻冲剂可有效减轻皮肤屏障损伤和炎症反应。LQZ的抗ad特性可能与抑制fc γ r介导的吞噬途径有关。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Liangxue Qushi Zhiyang Decoction Inhibits Atopic Dermatitis in Mice via FcγR-Mediated Phagocytosis.

Background: Liangxue Qushi Zhiyang Decoction (LQZ) is a traditional formula known for its efficacy in treating Atopic Dermatitis (AD). However, the specific mechanisms through which LQZ alleviates AD symptoms remain largely unknown. The objective of this study is to investigate the protective effects of LQZ on AD and to uncover its potential mechanisms of action. Methods: An AD model was established in mice using 2,4-dinitrochlorobenzene (DNCB). Mice were then orally administered LQZ or prednisolone (PDN). Throughout the treatment period, dermatitis scores and scratching frequencies of the mice were regularly monitored. Histopathological analyses were conducted using hematoxylin and eosin (H&E) staining and toluidine blue (TB) staining. Serum levels of inflammatory cytokines were measured using enzyme-linked immunosorbent assay (ELISA). Further, tandem mass tag (TMT) labeling quantitative proteomics was employed to identify differentially expressed proteins (DEPs). Enrichment analysis was conducted to pinpoint potential targets and pathways involved in LQZ's therapeutic action. Finally, validation experiments were performed to further explore the specific pathways and core targets of LQZ in AD treatment.. Results: LQZ treatment notably mitigated the skin barrier damage and inflammatory response induced by DNCB in AD mice, and reduced the serum levels of IgE, IL-4, and IL-1β. Proteomic analysis identified 248 proteins with differential expression, implicating multiple pathways in LQZ' therapeutic action. Among these, the Fc gamma R(FcγR)-mediated phagocytosis pathway emerged as a crucial factor in AD's inflammatory and immune responses. Key proteins associated with this pathway, including Fc-gamma RIII (Fcgr3), V-yes-1 Yamaguchi sarcoma viral related oncogene homolog (Lyn), Tyrosine-protein kinase (Syk), Phosphoinositide phospholipase C-gamma-2 (Plcg2), Neutrophil cytosol factor 1 (Ncf1), Ras-related C3 botulinum toxin substrate 2 (Rac2) and Actin-related protein 2/3 complex subunit 3 (Arpc3), exhibited significantly reduced expression levels following LQZ treatment. Conclusion: LQZ is effective in treating AD by alleviating skin barrier damage and inflammatory reactions. Its anti-AD properties of LQZ may be attributed to the inhibition of the FcγR-mediated phagocytic pathway.

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来源期刊
Mediators of Inflammation
Mediators of Inflammation 医学-免疫学
CiteScore
8.70
自引率
0.00%
发文量
202
审稿时长
4 months
期刊介绍: Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.
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