口疮黏附散通过NF-κB信号通路抑制醋酸诱导大鼠口腔溃疡

Aphthous ulcer Nianfu Powder prevents acetic acid-induced oral ulcers in rats via NF-κB signaling pathway

关键词:  口疮黏附散  口腔溃疡  NF-κB信号通路  免疫调控  分子机制

Key words:  Aphthous ulcer Nianfu Powder  Aphthous ulcer  NF-κB signaling pathway  Immune regulation  Molecular mechanism

摘要:

目的：本研究旨在探究加味口疮黏附散（Aphthous ulcer Nianfu Powder，MKNP）对醋酸诱导大鼠口腔溃疡的治疗效果及其潜在分子机制。 方法：首先，在HERB和Diseases数据库中检索MKNP复方药材的化学成分与靶基因以及口腔溃疡的相关靶基因，并通过交集处理找到候选靶基因。然后，利用g:Profiler对这些基因进行富集分析，识别出主要的信号通路。此外，通过体外实验评估MKNP复方对口腔上皮细胞活性的影响，并在体内实验中观察其对醋酸诱导口腔溃疡大鼠模型的治疗效果与分子机制。 结果：网络药理学分析显示，MKNP可能主要通过调控核转录因子κB（nuclear factor kappa-B，NF-κB）等信号通路影响细胞增殖、凋亡、迁移及免疫炎症反应。动物实验结果表明，MKNP能显著降低醋酸诱导的口腔溃疡大鼠的黏膜损伤，并改善病理变化。增殖细胞核抗原（Proliferating cell nuclear antigen，PCNA）免疫组化染色显示，MKNP能促进口腔黏膜上皮细胞的增生恢复。此外，MKNP还能显著改善醋酸诱导的大鼠细胞炎症因子紊乱，抑制NF-κB信号通路的激活。 结论：MKNP复方通过调节NF-κB等关键信号通路，有效缓解醋酸诱导大鼠口腔溃疡的症状，并促进黏膜修复。这一发现为理解MKNP作用机制提供了重要线索，并为后续的药物开发和治疗策略优化奠定基础。

Abstract:

Objective: The aim of this study was to investigate the therapeutic effect of Aphthous ulcer adhesion powder (MKNP) on acetic acid-induced oral ulcers in rats and its potential molecular mechanism. Methods: Initially, the chemical components and target genes of MKNP compound herbs, as well as related target genes of oral ulcers, were searched in HERB and Diseases databases. Candidate target genes were identified through intersection processing. Subsequently, g:Profiler was utilized to enrich these genes and identify the major signaling pathways. Additionally, the impact of MKNP compound on oral epithelial cell activity was assessed in vitro, while the therapeutic effect and molecular mechanism of MKNP compound on an acetic acid-induced oral ulcer rat model were observed in vivo. Results: Network pharmacological analysis indicated that MKNP may influence cell proliferation, apoptosis, migration, and immunoinflammatory response by regulating nuclear factor kappa-B (NF-κB) signaling pathways. The outcomes of animal experiments demonstrated that MKNP significantly reduced mucosal damage and improved pathological changes in rats with oral ulcers induced by acetic acid. Proliferating cell nuclear antigen (PCNA) immunohistochemical staining revealed that MKNP promoted the proliferation and recovery of oral mucosal epithelial cells. Furthermore, MKNP effectively ameliorated the inflammatory factor disorder induced by acetate and inhibited the activation of the NF-κB signaling pathway in rats. Conclusion: MKNP can effectively alleviate symptoms of acetic acid-induced oral ulcers and promote mucosal repair in rats by regulating key signaling pathways such as NF-κB. These findings offer vital insights into the mechanism of action of MKNP, establishing a foundation for subsequent drug development and optimization of treatment strategies.