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Researchers at the Lanzhou Institute of Husbandry and Pharmaceutical Sciences, CAAS Reveal the Molecular Mechanism of Aspirin Eugenol Ester in Alleviating Gastric Mucosal Injury in Animals

2026/05/08

Recently, the Veterinary Chemical Drug Innovation Team from Lanzhou Institute of Husbandry and Pharmaceutical Sciences, a member unit of the National Veterinary Drug Industry Technology Innovation Alliance, made significant research progress by revealing the molecular mechanism through which Aspirin Eugenol Ester (AEE) alleviates gastric mucosal injury in animals via regulation of oxidative stress and inflammatory signaling pathways. The findings provide important scientific support for the development of novel veterinary anti-inflammatory and analgesic drugs with higher efficacy and lower toxicity. The study was published in the internationally recognized journal Antioxidants.

Gastrointestinal health plays a vital role in maintaining animal performance and production efficiency. Under modern intensive farming conditions, animals are frequently exposed to environmental stress, dietary changes, and disease challenges, all of which can contribute to gastrointestinal mucosal damage and negatively affect growth performance and overall health.

Although traditional non-steroidal anti-inflammatory drugs (NSAIDs) are widely used for their anti-inflammatory and analgesic effects, prolonged use often causes gastrointestinal irritation and mucosal injury, limiting their clinical application in animals.

Based on a prodrug design strategy, the research team successfully synthesized Aspirin Eugenol Ester (AEE) by esterifying aspirin with eugenol, a natural bioactive compound. This innovative approach achieved the dual effect of reducing toxicity while enhancing therapeutic efficacy.

Experimental results demonstrated that AEE significantly improved gastric mucosal histopathological damage, reduced oxidative stress levels, and effectively alleviated inflammatory responses.

Further mechanistic studies showed that AEE activates the Nrf-2/GPX4 signaling axis to enhance antioxidant defense and eliminate excessive reactive oxygen species (ROS). Meanwhile, AEE suppresses the NF-κB inflammatory signaling pathway, thereby reducing the release of pro-inflammatory cytokines. In addition, AEE upregulates tight junction protein expression, strengthening the gastric mucosal barrier and ultimately exerting a protective effect on gastric tissues.

This research provides a new perspective for the safer and greener development of veterinary anti-inflammatory drugs and offers promising solutions for improving gastrointestinal health management and sustainable livestock production.

The study was supported by the National Natural Science Foundation of China and the China Postdoctoral Science Foundation, among other funding programs.