Expression of Cyclooxygenase-2 in Uterine Myoma Model Rats and Its Influence on the Development of Uterine Myomas

Abstract

Objective: To explore the expression of cyclooxygenase-2 (COX-2) in Uterine Myomas (Ums) model rats and its effect on the development of Ums. Methods: Six rats were randomly selected from 18 rats and divided into the model and control groups, with three rats in each group. The UMs model was established in the model group. Serum estradiol (E₂), progesterone (P) and COX-2 expression in rat uterine tissues of both groups were detected, and the uterine tissue damage of UM rats was observed by hematoxylin-eosin (HE) staining. Then, the remaining nine rats were stochastically assigned to model, vehicle and Anti-COX-2 groups for UM modeling again, with three rats in each group. In the Anti-COX-2 group, the COX-2 small interfering RNA (siRNA) expression vector was injected into the tail vein. The other three rats were left untreated as the control group. After modeling, B-cell lymphoma-2 associated X (Bax)/B-cell lymphoma-2 (Bcl-2) expression in rat uterus was detected, and the pathological changes of UM rats after silencing COX-2 were observed by Terminal Deoxynucleotidyl Transferase Mediated dUTP Nick End Labeling (TUNEL) and HE staining. Results: The model group showed higher E₂, P and COX-2 at messenger RNA (mRNA) and protein levels than the control group (p < 0.05), with obvious connective tissue hyperplasia, thickening of the uterine smooth muscle, and severe infiltration of inflammatory cells. The COX-2 and Bcl-2 protein levels in uterine tissue were lower, while the Bax protein was higher in the Anti-COX-2 group versus model and vehicle groups (p < 0.05). TUNEL and HE staining identified an increased number of positive cells in the Anti-COX-2 group, obviously decreased area of smooth muscle hyperplasia, neatly arranged smooth muscle cells, and decreased infiltration of inflammatory cells. Conclusions: COX-2 is expressed at a higher level in UMs. After silencing COX-2, UMs cell apoptosis is increased and tissue damage is significantly improved in UM rats, suggesting that COX-2 plays a vital role in the occurrence and development of UM.