Empagliflozin protects against indomethacin-induced gastric injury in rats: evidence from inflammatory, apoptotic, and early PI3K/Akt/VEGF-related changes
Abstract
Non-steroidal anti-inflammatory drugs (NSAIDs), particularly indomethacin, are widely used for the treatment of pain and inflammation but frequently cause gastric mucosal injury. Empagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor primarily used for type 2 diabetes, has recently attracted attention due to its anti-inflammatory, antioxidant, and cytoprotective properties. The present study investigated the potential gastroprotective effects of empagliflozin against indomethacin-induced gastric injury in rats and explored the underlying mechanisms related to inflammation, oxidative stress, apoptosis, and PI3K/Akt/VEGF-related signaling pathways. Male Sprague-Dawley rats were divided into six groups: control, indomethacin, indomethacin + famotidine, indomethacin + empagliflozin (10 mg/kg), indomethacin + empagliflozin (20 mg/kg), and empagliflozin (20 mg/kg). Rats were pretreated with empagliflozin for 7 days before induction of acute gastric injury with indomethacin. Gastric tissues were evaluated using biochemical, histopathological, immunohistochemical, and Western blot analyses. Indomethacin administration significantly increased pro-inflammatory cytokines (TNF-α and IL-6), reduced prostaglandin E2 levels, and increased cleaved caspase-3 expression, indicating activation of inflammatory and apoptotic pathways. Empagliflozin treatment significantly reduced inflammatory cytokine levels, restored prostaglandin levels, and suppressed cleaved caspase-3 expression,…
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