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<p>Stachydrine, a major bioactive alkaloid extracted from <i>Leonurus heterophyllus</i>, is a key component of traditional herbal medicine, recognized for its anti-inflammatory and antioxidant properties. In this study, we investigated the gastroprotective effects of stachydrine and its underlying mechanisms in a mouse model of indomethacin (IND)-induced gastric injury. Mice were intragastrically administered IND at a dose of 40&#xa0;mg/kg, followed 30&#xa0;min later by treatment with varying doses of stachydrine (0, 5, and 10&#xa0;mg/kg). Six hours post-IND administration, animals were sacrificed for further analysis. The results demonstrated that stachydrine treatment effectively attenuated IND-induced acute gastric injury, as evidenced by reduced gastric myeloperoxidase activity, and pro-inflammatory cytokine production (TNF-α, IL-6, and IL-1β). Stachydrine also significantly decreased gastric malondialdehyde activity while enhancing superoxide dismutase activity. Furthermore, it suppressed the expression of extracellular signal-regulated kinase (ERK), protein kinase B (AKT), and inducible nitric oxide synthase (iNOS) expressions. These findings indicate that stachydrine confers gastroprotection against IND-induced gastric injury, potentially by suppressing inflammatory and oxidative stress responses, inhibiting the ERK, AKT and iNOS signaling pathways. Thus, stachydrine may serve as a promising candidate for the treatment of IND-induced gastric injury.</p>

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Gastroprotective and antioxidant effects of stachydrine against indomethacin-induced gastric injury via ERK, AKT and iNOS signaling pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月2日

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  • Fu-Chao Liu,
  • Huang-Ping Yu,
  • Hung-Chen Lee,
  • Huan-Tang Lin,
  • Chia-Chih Liao

摘要

Stachydrine, a major bioactive alkaloid extracted from Leonurus heterophyllus, is a key component of traditional herbal medicine, recognized for its anti-inflammatory and antioxidant properties. In this study, we investigated the gastroprotective effects of stachydrine and its underlying mechanisms in a mouse model of indomethacin (IND)-induced gastric injury. Mice were intragastrically administered IND at a dose of 40 mg/kg, followed 30 min later by treatment with varying doses of stachydrine (0, 5, and 10 mg/kg). Six hours post-IND administration, animals were sacrificed for further analysis. The results demonstrated that stachydrine treatment effectively attenuated IND-induced acute gastric injury, as evidenced by reduced gastric myeloperoxidase activity, and pro-inflammatory cytokine production (TNF-α, IL-6, and IL-1β). Stachydrine also significantly decreased gastric malondialdehyde activity while enhancing superoxide dismutase activity. Furthermore, it suppressed the expression of extracellular signal-regulated kinase (ERK), protein kinase B (AKT), and inducible nitric oxide synthase (iNOS) expressions. These findings indicate that stachydrine confers gastroprotection against IND-induced gastric injury, potentially by suppressing inflammatory and oxidative stress responses, inhibiting the ERK, AKT and iNOS signaling pathways. Thus, stachydrine may serve as a promising candidate for the treatment of IND-induced gastric injury.