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

Abstract

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.