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<p>Diclofenac, a commonly prescribed NSAID, is frequently associated with gastric ulcer development. Emodin, a natural anthraquinone derivative, exhibits robust anti-inflammatory and antioxidant properties that may offer gastroprotective benefits. This study aimed to evaluate the protective and therapeutic effects of emodin on diclofenac-induced gastric ulcers in rats. A total of 56 male Wistar rats were randomly divided into seven groups (<i>n</i> = 8 each): healthy control, pre-induction, post-induction, pre-emodin, post-emodin, pre-esomeprazole, and post-esomeprazole. Gastric ulcers were induced with diclofenac (100&#xa0;mg/kg), and emodin (10&#xa0;mg/kg) or esomeprazole (20&#xa0;mg/kg) was administered orally for 14&#xa0;days, either before or after ulcer induction. Pre- and post-treatment with emodin significantly reduced ulcer indices, preserved mucosal integrity, and improved gastric pH, PGE2, and COX-1 levels, while decreasing gastric juice volume, pepsin, asymmetric dimethylarginine (ADMA), and alpha-1 antitrypsin (α1ATP). Emodin also attenuated oxidative stress, enhanced antioxidant defenses, reduced IL-6, and increased IL-10. Notably, it promoted angiogenesis via elevated VEGF and HGF and normalized diclofenac-induced histological alterations, supporting tissue repair. Emodin demonstrates potent gastroprotective and therapeutic effects against diclofenac-induced ulcers by modulating oxidative, inflammatory, and angiogenic pathways, highlighting its potential as a natural alternative to standard anti-ulcer therapy.</p>

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Gastroprotective and therapeutic effects of emodin on rat model of diclofenac-induced gastric ulceration

  • 期刊论文

  • 发表日期：

    2025年10月22日

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  • Samer Jaffar Sharif,
  • Haitham Mahmood Kadhim,
  • Basim Shehab Ahmed,
  • Hayder Ridha-Salman

摘要

Diclofenac, a commonly prescribed NSAID, is frequently associated with gastric ulcer development. Emodin, a natural anthraquinone derivative, exhibits robust anti-inflammatory and antioxidant properties that may offer gastroprotective benefits. This study aimed to evaluate the protective and therapeutic effects of emodin on diclofenac-induced gastric ulcers in rats. A total of 56 male Wistar rats were randomly divided into seven groups (n = 8 each): healthy control, pre-induction, post-induction, pre-emodin, post-emodin, pre-esomeprazole, and post-esomeprazole. Gastric ulcers were induced with diclofenac (100 mg/kg), and emodin (10 mg/kg) or esomeprazole (20 mg/kg) was administered orally for 14 days, either before or after ulcer induction. Pre- and post-treatment with emodin significantly reduced ulcer indices, preserved mucosal integrity, and improved gastric pH, PGE2, and COX-1 levels, while decreasing gastric juice volume, pepsin, asymmetric dimethylarginine (ADMA), and alpha-1 antitrypsin (α1ATP). Emodin also attenuated oxidative stress, enhanced antioxidant defenses, reduced IL-6, and increased IL-10. Notably, it promoted angiogenesis via elevated VEGF and HGF and normalized diclofenac-induced histological alterations, supporting tissue repair. Emodin demonstrates potent gastroprotective and therapeutic effects against diclofenac-induced ulcers by modulating oxidative, inflammatory, and angiogenic pathways, highlighting its potential as a natural alternative to standard anti-ulcer therapy.