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Objective <p>To compare the effectiveness of electroacupuncture (EA) combined with omeprazole (Ome) and Ome alone on indomethacin-induced gastric injury mice and reveal the underlying mechanism of this combination.</p> Methods <p>Fourty-eight male C57BL/6J mice were randomly divided into 6 groups by a simple random method (<i>n</i>=8), including control, model, Ome, Ome + EA, Ome + sham EA, and Ome + EA + ML385 groups. A gastric ulcer mouse model was constructed by intragastrically administering indomethacin at a dose of 30 mg/kg. EA and Ome treatment were performed twice daily with each session of EA treatment lasting 20 min. Gastric injury severity was determined by measuring the ulcer index. Sixteen mice with gastric ulcers underwent left cervical vagotomy (CV) were further divided into model + CV and Ome + EA + CV groups. Eight mice with gastric ulcers underwent sham vagotomy and EA combined with Ome treatment were included in the Ome + EA + SCV group. Following respective treatments, the gastric mucosal ulcer tissues were collected and pathologic scores were evaluated by HE staining. Oxygenase-1/tumor necrosis factor-α levels in gastric tissue were measured using ELISA. Colorimetric assay was conducted to measure oxidative stress levels. Real-time polymerase chain reaction was applied to detect the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) in gastric tissue. Immunofluorescence staining was performed to observe the locations and expressions of F4-80 and Nrf2 in the gastric mucosa. CV was conducted to evaluate the role of the vagus nerve in EA-mediated gastric injury improvement.</p> Results <p>EA combined with Ome alleviated gastric ulcers and decreased gastric pathologic scores (both <i>P</i>&lt;0.01). Furthermore, it decreased gastric oxidative stress levels and inhibited macrophages activation (all <i>P</i>&lt;0.01). However, vagotomy abolished the antioxidant function of EA. Meanwhile, we observed that Nrf2 plays a critical role in inducing the therapeutic effect of EA combined with Ome on gastric injury.</p> Conclusion <p>In mice with gastric ulcers, EA combined with Ome can better repair indomethacin-induced gastric injury via inactivation of macrophages and Nrf2-mediated antioxidant signaling pathway, which is primarily mediated by vagus nerve.</p>

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Electroacupuncture Enhances Effectiveness of Omeprazole in Indomethacin-Induced Gastric Injury Mice via Nrf2 Activation and Vagus Nerve Conduction

  • 期刊论文

  • 发表日期：

    2026年4月1日

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  • Yu-jun Hou,
  • Wen Wang,
  • Jiang-nan Ye,
  • Lu Wang,
  • Si-yuan Zhou,
  • Yun-zhou Shi,
  • Ying Chen,
  • Jun-peng Yao,
  • Lu-qiang Sun,
  • Ying Li

摘要

Objective

To compare the effectiveness of electroacupuncture (EA) combined with omeprazole (Ome) and Ome alone on indomethacin-induced gastric injury mice and reveal the underlying mechanism of this combination.

Methods

Fourty-eight male C57BL/6J mice were randomly divided into 6 groups by a simple random method (n=8), including control, model, Ome, Ome + EA, Ome + sham EA, and Ome + EA + ML385 groups. A gastric ulcer mouse model was constructed by intragastrically administering indomethacin at a dose of 30 mg/kg. EA and Ome treatment were performed twice daily with each session of EA treatment lasting 20 min. Gastric injury severity was determined by measuring the ulcer index. Sixteen mice with gastric ulcers underwent left cervical vagotomy (CV) were further divided into model + CV and Ome + EA + CV groups. Eight mice with gastric ulcers underwent sham vagotomy and EA combined with Ome treatment were included in the Ome + EA + SCV group. Following respective treatments, the gastric mucosal ulcer tissues were collected and pathologic scores were evaluated by HE staining. Oxygenase-1/tumor necrosis factor-α levels in gastric tissue were measured using ELISA. Colorimetric assay was conducted to measure oxidative stress levels. Real-time polymerase chain reaction was applied to detect the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) in gastric tissue. Immunofluorescence staining was performed to observe the locations and expressions of F4-80 and Nrf2 in the gastric mucosa. CV was conducted to evaluate the role of the vagus nerve in EA-mediated gastric injury improvement.

Results

EA combined with Ome alleviated gastric ulcers and decreased gastric pathologic scores (both P<0.01). Furthermore, it decreased gastric oxidative stress levels and inhibited macrophages activation (all P<0.01). However, vagotomy abolished the antioxidant function of EA. Meanwhile, we observed that Nrf2 plays a critical role in inducing the therapeutic effect of EA combined with Ome on gastric injury.

Conclusion

In mice with gastric ulcers, EA combined with Ome can better repair indomethacin-induced gastric injury via inactivation of macrophages and Nrf2-mediated antioxidant signaling pathway, which is primarily mediated by vagus nerve.