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Protective effects of polydatin on LPS-induced endometritis in mice
- Li, Rong, Maimai, T., Yao, Hongmei, Liu, Xueshibojie, He, Zhaoqi, Xiao, Chong, Wang, Yinan, Xie, Guanghong
- Microbial pathogenesis 2019 v.137 pp. 103720
- Reynoutria japonica, animal models, antioxidant activity, dose response, endometritis, enzyme-linked immunosorbent assay, histopathology, humans, inflammation, interleukin-1beta, interleukin-6, lipopolysaccharides, mice, myeloperoxidase, polyphenols, protective effect, rhizomes, signal transduction, staining, transcription factor NF-kappa B, tumor necrosis factor-alpha, uterine tissue, vagina
- Endometritis, a common inflammation of the uterus, often causes severe damage to human and animal reproductive health. Polydatin is a polyphenol extracted from the rhizome of Polygonum cuspidatum that has anti-inflammatory and anti-oxidative effects. The purpose of this study was to investigate the underlying protective effects and mechanisms of polydatin against lipopolysaccharide (LPS)-induced endometritis in mice. The mouse model of endometritis was established by injection of LPS through the vagina. The uterine tissues of each group were gathered to analyze histopathological changes, inflammatory cytokine production, and the degree of activation of the NF-κB and Nrf2 signaling pathways. The myeloperoxidase (MPO) activity assay indicated that polydatin treatment significantly alleviated inflammatory cell infiltration in LPS-induced endometritis mice. Furthermore, polydatin treatment remarkably impeded the expression of TNF-α, IL-1β, and IL-6 by ELISA assay. Hematoxylin-eosin staining (H&E) showed that polydatin significantly decreased impairment of the uterus. In addition, polydatin was also found to suppress LPS-induced NF-κB activation in a dose-dependent manner. The expression of Nrf2 and HO-1 was enhanced by polydatin treatment. All the results suggest that polydatin helpfully alleviates LPS-induced endometritis by suppressing the NF-ĸB signaling pathway and activating the Nrf2 signaling pathway.