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Aspirin or ethanol induced gastric ulcer rat models are the most frequently used in studies. Aspirin and ethanol induced gastric ulcers through different pathways involving COX-2 and iNOS. The aim of this study was to examine the expression of COX-2 and iNOS in gastric ulcer rat model induced by ethanol and aspirin. Twenty-one Sprague Dawley rats were divided into 7 groups i.e. control group (CA), ethanol 1st day (ED1), ethanol 3rd day (ED3), ethanol 5th day (ED5), aspirin 4th day (AD4), aspirin 6th day (AD6), and aspirin 8th day (AD8). Oral administration of aspirin was at 200mg/kgBW and the 100% ethanol at 1mL/200gBW. Macroscopic and microscopic observations were done to examine the gastric mucosal damage, COX-2 and iNOS expressions. Severe gastric ulcers were observed in ED1 and AD4 groups and mild gastric mucosal damage was observed in ED3, ED5, AD6 and AD8 groups. Microscopically, light erosion was shown by the CA and AD8 groups. Erosion was also shown by ED3, ED5, and AD6 groups. The most severe damage with ulcers and heavier bleeding were shown by the ED1 and AD4 groups. Weak COX-2 expression was found in the CA, while the highest COX-2 expression was found in the ED1. The iNOS expression in the ethanol groups was still increasing until the 5th day (ED5). In the aspirin groups, it reached the peak on the 3rd day (AD6), and already declined on the 5th day (AD8). In conclusion, the damage process of ethanol induced gastric ulcer occurred faster than that by aspirin. The highest COX-2 expression in the ethanol and aspirin groups were shown at the onset begin. iNOS expression in ethanol induced ulcer groups still increased until the 5th day, while in the aspirin induced ulcer groups already declined in the 5th day.

The expression of COX-2 and iNOS in ethanol and aspirin induced gastric ulcer rat models