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Endometritis is the inflammatory response of the uterine lining which is linked to infertility. Administration of platelet-rich plasma (PRP) represents a well-recommended strategy for the treatment of endometrium-associated infertility. In this study, we set to characterize the role and molecular mechanism of PRP intrauterine infusion in mice with endometritis. A mouse model of endometritis was established using lipopolysaccharide (LPS). Mouse endometrial epithelial cells were obtained in primary culture. PRP-treated cells were assayed for proliferative and apoptotic activities. Moreover, iNOS expression and chemokine and inflammatory factor contents in cells were assessed using RT-qPCR and ELISA. The mice were subjected to PRP intrauterine infusion. The expression of genes related to uterine development was analyzed by qPCR and the ki-67 content and caspase-3 activation in endometrial tissues were examined by immunohistochemistry. Finally, the Nrf2/HO-1 pathway activity in tissues was examined by Western blot. LPS induced inflammatory cell recruitment and tissue damage in the endometrium of mice, along with significantly increased levels of inflammatory and chemokine factors. PRP significantly enhanced endometrial epithelial cell activity, decreased apoptosis, and reduced inflammatory factor secretion. In addition, PRP intrauterine infusion significantly increased the expression of genes related to uterine development, promoted tissue proliferation, decreased apoptosis, and diminished inflammatory response in endometrial tissues of mice. PRP intrauterine infusion significantly elevated Nrf2/HO-1 pathway activity in endometrial epithelial cells and tissues. PRP intrauterine infusion significantly inhibited endometrial cell injury and alleviated the inflammatory response through activating the Nrf2/HO-1 pathway.

immunopharmacology and immunotoxicology

Nrf2/HO-1 pathway is involved the anti-inflammatory action of intrauterine infusion of platelet-rich plasma against lipopolysaccharides in endometritis