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<p>Syringaldehyde (SG) is a naturally derived phenolic aldehyde known for a range of biological activities. This study evaluated its protective potential against the chemically induced gastric injury model and investigated the underlying mechanisms involved. Acute gastric ulceration was induced in male Swiss albino mice by intragastric administration of a mixture of 0.3&#xa0;M HCl and 70% ethanol. SG was orally administered at 25 and 50&#xa0;mg/kg, and omeprazole (20&#xa0;mg/kg) served as the reference anti-ulcer drug. HCl/ethanol exposure caused severe gastric mucosal injury characterized by increased lipid peroxidation, elevated levels of inflammatory mediators (IL-6, NFκB, iNOS, Cox-2, TNF-α, and IL-1β), and enhanced pro-apoptotic markers Bax and Cas-3. In parallel, antioxidant defense mechanisms were markedly impaired, as indicated by decreased GSH levels, reduced SOD and CAT activities, diminished mucosal protective mediators (PGE2 and NO), and downregulation of HO-1, Nrf2, and Bcl-2 expression. Treatment with SG significantly attenuated oxidative stress, gastric mucosal damage, and inflammatory responses, and modulated apoptosis-related markers. These protective effects were accompanied by restoration of antioxidant enzyme activities and increased levels of PGE2 and NO, together with upregulation of Nrf2/HO-1 expression. Overall, these results suggest that SG may exert gastroprotective effects against gastric injury through modulation of oxidative stress, inflammation, and apoptotic pathways.</p>

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Syringaldehyde inhibits NFκB-mediated inflammation and apoptosis and activates Nrf2/HO-1 signaling to reduce HCl/ethanol-induced gastric injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月26日

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  • Berrin Yalinbas-Kaya,
  • Selcan Cesur,
  • Sinan Ince

摘要

Syringaldehyde (SG) is a naturally derived phenolic aldehyde known for a range of biological activities. This study evaluated its protective potential against the chemically induced gastric injury model and investigated the underlying mechanisms involved. Acute gastric ulceration was induced in male Swiss albino mice by intragastric administration of a mixture of 0.3 M HCl and 70% ethanol. SG was orally administered at 25 and 50 mg/kg, and omeprazole (20 mg/kg) served as the reference anti-ulcer drug. HCl/ethanol exposure caused severe gastric mucosal injury characterized by increased lipid peroxidation, elevated levels of inflammatory mediators (IL-6, NFκB, iNOS, Cox-2, TNF-α, and IL-1β), and enhanced pro-apoptotic markers Bax and Cas-3. In parallel, antioxidant defense mechanisms were markedly impaired, as indicated by decreased GSH levels, reduced SOD and CAT activities, diminished mucosal protective mediators (PGE2 and NO), and downregulation of HO-1, Nrf2, and Bcl-2 expression. Treatment with SG significantly attenuated oxidative stress, gastric mucosal damage, and inflammatory responses, and modulated apoptosis-related markers. These protective effects were accompanied by restoration of antioxidant enzyme activities and increased levels of PGE2 and NO, together with upregulation of Nrf2/HO-1 expression. Overall, these results suggest that SG may exert gastroprotective effects against gastric injury through modulation of oxidative stress, inflammation, and apoptotic pathways.