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Research Article
Jianji Li
Yangzhou University
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Postpartum uterine infection can lead to endometrial inflammation and oxidative damage. Progesterone makes the animal more susceptible to uterine infection. Progesterone has been proved to play an anti-inflammatory role in inhibiting uterine innate immunity, and to reduce tissue oxidative damage. But the effect of progesterone on the oxidative damage of bovine endometrium has not been reported. The purpose of this study was to explore the effect and mechanism of progesterone (1, 3, and 5 ng/mL) on oxidative damage in primary bovine endometrial epithelial cells (BEEC) induced by lipopolysaccharide (LPS) from Escherichia coli.
Results
Compared with the LPS group, there were decreases (P < 0.05) in the levels of reactive oxygen and malondialdehyde, and increases (P < 0.05) in the activities of superoxide dismutase and catalase, and total antioxidant capacity in the cotreatment groups of progesterone and LPS. The cotreatment of LPS and P4 upregulated (P < 0.05) the mRNA abundance of antioxidant genes and the key protein levels in Nrf2/Keap1 pathway, and promoted the Nrf2 protein to enter the nucleus. The use of progesterone receptor antagonist mifepristone reversed the antioxidative effect of progesterone.
Conclusions
Progesterone protects BEEC from LPS-induced oxidative damage by activating Nrf2/Keap1 pathway through progesterone receptor.
Keywords
progesterone, oxidative stress, lipopolysaccharide, bovine endometrial epithelial cells, Nrf2/Keap1
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No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research Article
Jianji Li
Yangzhou University
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 02 Nov, 2021
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Veterinary Epidemiology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
Postpartum uterine infection can lead to endometrial inflammation and oxidative damage. Progesterone makes the animal more susceptible to uterine infection. Progesterone has been proved to play an anti-inflammatory role in inhibiting uterine innate immunity, and to reduce tissue oxidative damage. But the effect of progesterone on the oxidative damage of bovine endometrium has not been reported. The purpose of this study was to explore the effect and mechanism of progesterone (1, 3, and 5 ng/mL) on oxidative damage in primary bovine endometrial epithelial cells (BEEC) induced by lipopolysaccharide (LPS) from Escherichia coli.
Results
Compared with the LPS group, there were decreases (P < 0.05) in the levels of reactive oxygen and malondialdehyde, and increases (P < 0.05) in the activities of superoxide dismutase and catalase, and total antioxidant capacity in the cotreatment groups of progesterone and LPS. The cotreatment of LPS and P4 upregulated (P < 0.05) the mRNA abundance of antioxidant genes and the key protein levels in Nrf2/Keap1 pathway, and promoted the Nrf2 protein to enter the nucleus. The use of progesterone receptor antagonist mifepristone reversed the antioxidative effect of progesterone.
Conclusions
Progesterone protects BEEC from LPS-induced oxidative damage by activating Nrf2/Keap1 pathway through progesterone receptor.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
Figure 6
Figure 7
Figure 8
Figure 9
No competing interests reported.
This is a list of supplementary files associated with this preprint. Click to download.
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