Scholarlink

Background <p>Peptic ulcer disease is a common gastrointestinal disorder caused by an imbalance between damaging factors and mucosal protection. Alcohol induces gastric injury through oxidative stress, inflammation, and apoptosis, while phenytoin may have potential preventive effects in ulcer. This study aimed to evaluate the gastroprotective effects of phenytoin against ethanol-induced gastric ulcers in rats, focusing on oxidative stress, inflammatory, and apoptotic biomarkers, and to elucidate the underlying molecular mechanisms.</p> Methods <p>Thirty-two male Wistar rats were randomly divided into four groups: control, ethanol-induced gastric ulcer (ETH), phenytoin-treated (ETH + Phen), and omeprazole-treated (ETH + Ome). Gastric ulcers were induced by oral administration of absolute ethanol. Ulcer area, gastric content volume, oxidative stress markers (TAC, MDA, GSH, SOD, CAT), inflammatory mediators (NF-κB, TNF-α, IL-1β, iNOS, COX-2), and apoptotic markers (Bax, Bcl-2, Caspase-3) were measured using biochemical assays, real time PCR, and ELISA.</p> Results <p>Ethanol administration significantly increased ulcer area, gastric content volume, MDA levels, NF-κB activation, pro-inflammatory cytokines, and pro-apoptotic markers, while reducing TAC, GSH, and antioxidant enzyme activities. Preventive phenytoin treatment significantly attenuated these effects, reducing ulcer area, restoring antioxidant balance, suppressing NF-κB-mediated inflammation, and modulating apoptotic signaling. Both phenytoin and omeprazole improved these parameters compared with the ethanol group; however, no direct statistical comparison between the two treatments was performed.</p> Conclusion <p>Phenytoin exhibits significant gastroprotective effects against ethanol-induced gastric injury, which may be associated with modulation of oxidative stress, inflammatory pathways, and apoptosis.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Effects of phenytoin on ethanol-induced gastric ulceration in rats: involvement of oxidative stress, inflammation, and apoptosis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月3日

查看全文
  • Kaveh Rahimi,
  • Masoud Najafi,
  • Shahrzad Fayazfard,
  • Mehdi Esmaeili

摘要

Background

Peptic ulcer disease is a common gastrointestinal disorder caused by an imbalance between damaging factors and mucosal protection. Alcohol induces gastric injury through oxidative stress, inflammation, and apoptosis, while phenytoin may have potential preventive effects in ulcer. This study aimed to evaluate the gastroprotective effects of phenytoin against ethanol-induced gastric ulcers in rats, focusing on oxidative stress, inflammatory, and apoptotic biomarkers, and to elucidate the underlying molecular mechanisms.

Methods

Thirty-two male Wistar rats were randomly divided into four groups: control, ethanol-induced gastric ulcer (ETH), phenytoin-treated (ETH + Phen), and omeprazole-treated (ETH + Ome). Gastric ulcers were induced by oral administration of absolute ethanol. Ulcer area, gastric content volume, oxidative stress markers (TAC, MDA, GSH, SOD, CAT), inflammatory mediators (NF-κB, TNF-α, IL-1β, iNOS, COX-2), and apoptotic markers (Bax, Bcl-2, Caspase-3) were measured using biochemical assays, real time PCR, and ELISA.

Results

Ethanol administration significantly increased ulcer area, gastric content volume, MDA levels, NF-κB activation, pro-inflammatory cytokines, and pro-apoptotic markers, while reducing TAC, GSH, and antioxidant enzyme activities. Preventive phenytoin treatment significantly attenuated these effects, reducing ulcer area, restoring antioxidant balance, suppressing NF-κB-mediated inflammation, and modulating apoptotic signaling. Both phenytoin and omeprazole improved these parameters compared with the ethanol group; however, no direct statistical comparison between the two treatments was performed.

Conclusion

Phenytoin exhibits significant gastroprotective effects against ethanol-induced gastric injury, which may be associated with modulation of oxidative stress, inflammatory pathways, and apoptosis.