ABSTRACT
Objective The pathogenesis of orla ulcer has not been fully and thoroughly studied. This study aimed to investi-gate the effect and mechanism of Rosmarinic acid (RA)on oral ulcer. Methods 60 SD rats were randomly divided into control group,model group,RA groups(20,40,80 mg/kg) and Watermelon Frost group. The control group rats were fed normally and with-out any treatment. The oral ulcer model was established in the other three groups. The oral ulcer model of rat was established by injec-tion of 40% glacial acetic acid on the oral mucosa of cheek in rat. One day after the formation of ulcers,RA(20,40,80 mg/kg) and watermelon frost (200 mg/kg) was administrated. The ulcer area was measured 3,5,7 days after establishing the model. The concen-tration of IL-18 and IL-1β in ulcer tissue was measured by ELISA method and the expression of NLRP3 mRNA was measured by qRT-PCR. Results Compared with the model group, the ulcer area in the RA group and Watermelon Frost group was significantly de-ceased(P<0.05). Compared with the control group,NLRP3,IL-18 and IL-1β in the ulcer tissue was significantly elevated in model group,RA groups (20,40,80 mg/kg) and Watermelon Frost group (P<0.01). NLRP3 expressed lower in RA (40,80 mg/kg) and wa-termelon frost (200 mg/kg) group(5.27 ± 0.53, 3.25 ± 0.46, 4.75 ± 0.51) than in model group(8.71±0.35)( P<0.05). IL-18 expressed lower in RA (40, 80 mg/kg) and watermelon frost (200 mg/kg) group [(174.21±18.21), (110.12±14.23), (142.25±12.61) pg/mL] than in model group [(246.21±26.21) pg/mL](P<0.05). IL-1β expressed lower in RA (40, 80 mg/kg) and watermelon frost(200 mg/kg) group [(94.76±7.26),(81.77±7.80),(90.21±8.71) pg/mL] than in model group [(133.01±11.69) pg/mL](P<0.05). Conclusion RA has some therapeutic effect on oral ulcers,the mechanism may be related to NLRP3.