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Updated: May 20, 2025

Intraductal Injection of LPS as a Mouse Model of Mastitis: Signaling Visualized via an NF-κB Reporter Transgenic
Published on: September 4, 2012
Fucoxanthin attenuates LPS-induced endometritis via inhibiting inflammatory factors through the NF-κB pathway
Qin Yao1, Yuejuan Zhang1, Qizhi Yan1
1Department of Pharmacy, Shaoxing People's Hospital, Shaoxing 312000, China.
Abstract:
Endometritis is an infectious disease of the female reproductive system and commonly treated with antibiotics. However, the high resistance rates to antibiotics necessitate the urgent research for new and effective therapeutic strategies. The aim of this research is to explore the effect of fucoxanthin (FX) on endometritis through in vitro and in vivo assays. The effect of FX on inflammation was first explored in vitro using LPS-induced bovine endometrial epithelial (BEND) cell injury model. After the anti-inflammation effect of FX was confirmed in vitro, the effect of FX on endometritis was investigated in vivo using LPS-induced mice model. The female mice were randomly assigned into control, control + FX, LPS, and LPS + FX (100, 200 mg/kg) groups. The histological features of the uterus and expression levels of NF-κBp65 and inflammatory mediators (COX-2, iNOS, IL-1β, IL-6, and TNF-α) in the uterine tissue were compared among the animal groups. Our in vitro results showed that LPS induced BEND cell damage while significantly enhancing the expression of NF-κBp65 and inflammatory mediators (COX-2, iNOS, IL-1β, IL-6, and TNF-α). Nevertheless, pretreatment with FX reversed the abnormal phenomena caused by LPS. In vivo, LPS treatment resulted in obvious histopathological uterus damages, which were alleviated by FX treatment. Consistent with the in vitro assay, FX treatment also inhibited the expression of NF-κBp65 and inflammatory mediators in the animal experiments. Our study implies that FX is a potential therapeutic agent for endometritis. The beneficial function of FX on endometritis was achieved by inhibiting the inflammatory factors through the NF-κB pathway.
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