Phytomedicine : international journal of phytotherapy and phytopharmacology · 2026
Euodia rutaecarpa (Juss.) Benth. var. officinalis (Dode) Huang and evodiamine ameliorate N-methyl-N'-nitro-N-nitrosoguanidine-induced chronic atrophic gastritis in rats via the phosphatidylinositol 3-kinase/protein kinase B/nuclear factor kappa-B pathway.
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Wang Liping, Gao Feng, Tian Jingzhuo, Wang Lianmei, Zhao Yong, Liu Suyan, Yi Yan, Li Chunying, Liu Chenyue, Meng Jing, Zhang Yushi, Pan Chen, Han Jiayin, Liu Meiting, Wang Xingwen, Cui Shuang, Jia Liqun, Liang Aihua
Аннотация
BACKGROUND: Chronic atrophic gastritis (CAG) is a common chronic digestive disorder associated with the occurrence and development of gastric cancer (GC). Euodia rutaecarpa (Juss.) Benth. var. officinalis (Dode) Huang (Fructus evodiae) is a traditional Chinese medicinal material often used to treat gastrointestinal diseases. However, the therapeutical effects of Fructus evodiae in CAG and underlying mechanisms remain unelucidated.
PURPOSE: This study aimed to determine the efficacy of the water decoction of fructus evodiae in the treatment of CAG, reveal its mechanism of action, clarify its pharmacological material basis and regulatory pathways in the treatment of CAG, and provide a scientific basis for the clinical treatment of CAG with fructus evodiae.
METHOD: First, we established CAG rat model and administered fructus evodiae decoction for treatment, monitoring serum inflammatory factors, hormones, and histopathology. Then, components of fructus evodiae decoction were determined using UHPLC-Q Exactive Orbitrap HRMS. Subsequently, the mechanism of fructus evodiae in the treatment of CAG were explored by proteomics analysis, network pharmacology and molecular docking. Finally, in vivo and in vitro validation was taken by western blot (WB) assays, ELISA, CCK-8, immunofluorescence staining, hematoxylin and eosin (HE) measurement, bile acid (BAs) analysed.
RESULTS: Data showed that 25 compounds were identified in fructus evodiae decoction. The proteomics analysis, network pharmacology, and molecular docking results showed evodiamine (EVO) is a major active ingredient and PI3K/AKT/NF-κB pathway and gastrointestinal motility are key regulating pathways in fructus evodiae decoction used to treat CAG. In vivo and in vitro experiments confirmed that Fructus evodiae decoction and EVO significantly reduced the expression levels of IL-1β, IL-6, TNF-α, Gastrin-17 (G-17), somatostatin (SS), caudal type homeobox 2 (CDX2), and mucin 2 (MUC2) protein by inhibited PI3K/AKT/NF-κB signaling. Moreover, fructus evodiae decoction and EVO increased the expression of the gastrointestinal excitatory neurotransmitters ACh and 5-HT, promoted gastric emptying rate and small intestinal propulsion rate, and reduced the level of BAs in the stomach, thereby reducing further damage to the gastric mucosa.
CONCLUSION: Fructus evodiae decoction exerts anti-CAG effects primarily by suppressing chronic inflammation and intestinal metaplasia through inhibition of the PI3K/AKT/NF-κB signaling pathway, thereby reducing bile acid accumulation and restoring gastrointestinal function. Importantly, evodiamine was identified as a key bioactive alkaloid of Fructus evodiae and was further validated as a critical mediator of these effects via targeted in vivo and in vitro experiments. By integrating proteomics, network pharmacology, molecular docking, and single-compound mechanistic validation, this study establishes evodiamine-centered regulation of the PI3K/AKT/NF-κB axis as a unifying mechanism underlying the therapeutic action of Fructus evodiae in MNNG-induced chronic atrophic gastritis.
PURPOSE: This study aimed to determine the efficacy of the water decoction of fructus evodiae in the treatment of CAG, reveal its mechanism of action, clarify its pharmacological material basis and regulatory pathways in the treatment of CAG, and provide a scientific basis for the clinical treatment of CAG with fructus evodiae.
METHOD: First, we established CAG rat model and administered fructus evodiae decoction for treatment, monitoring serum inflammatory factors, hormones, and histopathology. Then, components of fructus evodiae decoction were determined using UHPLC-Q Exactive Orbitrap HRMS. Subsequently, the mechanism of fructus evodiae in the treatment of CAG were explored by proteomics analysis, network pharmacology and molecular docking. Finally, in vivo and in vitro validation was taken by western blot (WB) assays, ELISA, CCK-8, immunofluorescence staining, hematoxylin and eosin (HE) measurement, bile acid (BAs) analysed.
RESULTS: Data showed that 25 compounds were identified in fructus evodiae decoction. The proteomics analysis, network pharmacology, and molecular docking results showed evodiamine (EVO) is a major active ingredient and PI3K/AKT/NF-κB pathway and gastrointestinal motility are key regulating pathways in fructus evodiae decoction used to treat CAG. In vivo and in vitro experiments confirmed that Fructus evodiae decoction and EVO significantly reduced the expression levels of IL-1β, IL-6, TNF-α, Gastrin-17 (G-17), somatostatin (SS), caudal type homeobox 2 (CDX2), and mucin 2 (MUC2) protein by inhibited PI3K/AKT/NF-κB signaling. Moreover, fructus evodiae decoction and EVO increased the expression of the gastrointestinal excitatory neurotransmitters ACh and 5-HT, promoted gastric emptying rate and small intestinal propulsion rate, and reduced the level of BAs in the stomach, thereby reducing further damage to the gastric mucosa.
CONCLUSION: Fructus evodiae decoction exerts anti-CAG effects primarily by suppressing chronic inflammation and intestinal metaplasia through inhibition of the PI3K/AKT/NF-κB signaling pathway, thereby reducing bile acid accumulation and restoring gastrointestinal function. Importantly, evodiamine was identified as a key bioactive alkaloid of Fructus evodiae and was further validated as a critical mediator of these effects via targeted in vivo and in vitro experiments. By integrating proteomics, network pharmacology, molecular docking, and single-compound mechanistic validation, this study establishes evodiamine-centered regulation of the PI3K/AKT/NF-κB axis as a unifying mechanism underlying the therapeutic action of Fructus evodiae in MNNG-induced chronic atrophic gastritis.