Oxycodone alleviates mifepristone‐stimulated human endometrial stromal cell injury by activating the Keap1/Nrf2/HO‐1 signaling pathway

Abstract Background Endometrial injury is a common disease in women caused by intrauterine inflammation, infections, and endocrine disorders. Human endometrial stromal cells (hEndoSCs) can maintain homeostasis play an important role repairing injury. Mifepristone, steroidal anti‐progesterone drug, widely used the field of reproductive medicine worldwide. Mifepristone‐induced hEndoSC has been to study vitro. At present, pathogenesis potential regulatory mechanisms oxycodone remain unknown. Aims We aimed evaluate functions mifepristone‐stimulated analyze its molecular mechanism. Materials & Methods viability, cytotoxicity, apoptosis were analyzed using methyl thiazolyl tetrazolium assay, lactate dehydrogenase flow cytometry, respectively. Furthermore, levels cleaved‐Caspase3, Keap1, Nrf2, HO‐1, NQO1 assessed reverse transcription quantitative polymerase chain reaction western blot analysis, release inflammatory cytokines was determined enzyme‐linked immunosorbent assay. Results observed that had no adverse effects on hEndoSCs; rather, it protected hEndoSCs against mifepristone‐induced damage, as confirmed enhanced cell reduced number apoptotic cells, decreased Caspase3 activity cytokine secretion, increased Keap1/Nrf2/HO‐1 pathway‐related protein expression. In addition, we found protective inhibited ML385 (a inhibitor). Conclusion summary, alleviates activating signaling pathway.