فهرست نشریات علمی دسترسی آزاد ایران

The prevalence of dysmenorrhea in the world is still quite high. Primary dysmenorrhea occurs due to an increase in prostaglandin F2α (PGF2α). Cyclooxigenase-2 (COX-2) is a crucial component that controls the synthesis of prostaglandins. A key target for reducing menstrual pain is COX-2. This study aimed to investigate the effect of curcumin on COX-2 expression and PGF2α expression in uterine tissue in mice model primary dysmenorrhea. The study involved a randomized post-test control group design using non-pregnant female Balb/c mice as a model of primary dysmenorrhea induced by estradiol benzoate and oxytocin. Five groups of mice (n = 7 each group) were randomly assigned: Sham group (SG), which received placebo; Ibuprofen group (IG), which received ibuprofen 100 mg/kg; C100, which received 100 mg/kg of curcumin; C200, which received 200 mg/kg of curcumin; and C400, which received 400 mg/kg of curcumin. The intervention was administered orally twice a day for 7 days. For ten days, estradiol benzoate was injected subcutaneously, and on day 11, oxytocin was injected intraperitoneally. COX-2 expression was examined by Western blot and prostaglandin expression by immunohistochemistry. The data was analyzed using a one-way analysis of variance and Tukey's test. Curcumin significantly decreased COX-2 and PGF2α expression in uterine tissues of primary dysmenorrhea models compared with the SG (p<0.05). There is no significant difference in COX-2 and PGF2α expression between IG and C400 (p>0.05). Curcumin effectively reduces COX-2 and PGF2α expression in uterine tissues in mice models of primary dysmenorrhea.