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<p>Chronic atrophic gastritis (CAG) is regarded as a transitional stage in the progression from gastritis to gastric tumors. Although preserved egg white (PEW) is recognized for its anti-inflammatory properties, its precise impact and mechanisms in treating gastric inflammation are not fully understood. This study employed an integrative approach, combining network pharmacology with experimental validation, to elucidate the therapeutic effects of PEW on CAG and its underlying mechanisms. Through network pharmacology, potential targets and associated signaling pathways were identified. The results indicated that peptides within PEW were involved in CAG intervention alongside 61 targets. KEGG enrichment analysis unveiled 99 signaling pathways. Molecular docking revealed favorable binding properties between PEW’s main active compounds and core targets. The model was established using the N-Methyl-N´-nitro-N-nitrosoguanidine (MNNG) comprehensive method. Cellular experiments demonstrated a significant reduction in the secretion of IL-6 (41.73%), IL-8 (20.35%), and TNF-α (31.49%)， while enhancing cell proliferation and motility (<i>P</i> &lt; 0.05). Animal experiments showed alignment of rat gastric tissue glands, increased pepsin activity, reduced inflammatory factors in serum, and regulation of Bcl-2 and NF-κB expression following PEW treatment. These findings collectively highlight PEW’s potential as a therapeutic intervention for CAG, presenting a promising alternative treatment approach.</p>

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Combining network pharmacology and experimental validation to investigate the role of preserved egg white in intervening in chronic atrophic gastritis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月15日

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  • Jingying Sun,
  • Yulin Wang,
  • Yuanyuan Zhang,
  • Yuxi Peng,
  • Wei Liu,
  • Xiaomeng Li,
  • Zhaoxia Cai,
  • Xi Huang,
  • Youyou Lu,
  • Long Sheng

摘要

Chronic atrophic gastritis (CAG) is regarded as a transitional stage in the progression from gastritis to gastric tumors. Although preserved egg white (PEW) is recognized for its anti-inflammatory properties, its precise impact and mechanisms in treating gastric inflammation are not fully understood. This study employed an integrative approach, combining network pharmacology with experimental validation, to elucidate the therapeutic effects of PEW on CAG and its underlying mechanisms. Through network pharmacology, potential targets and associated signaling pathways were identified. The results indicated that peptides within PEW were involved in CAG intervention alongside 61 targets. KEGG enrichment analysis unveiled 99 signaling pathways. Molecular docking revealed favorable binding properties between PEW’s main active compounds and core targets. The model was established using the N-Methyl-N´-nitro-N-nitrosoguanidine (MNNG) comprehensive method. Cellular experiments demonstrated a significant reduction in the secretion of IL-6 (41.73%), IL-8 (20.35%), and TNF-α (31.49%)， while enhancing cell proliferation and motility (P < 0.05). Animal experiments showed alignment of rat gastric tissue glands, increased pepsin activity, reduced inflammatory factors in serum, and regulation of Bcl-2 and NF-κB expression following PEW treatment. These findings collectively highlight PEW’s potential as a therapeutic intervention for CAG, presenting a promising alternative treatment approach.