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Schisandrin B Inhibits LPS‐Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway
Schisandrin B Inhibits LPS‐Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway
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Schisandrin B Inhibits LPS‐Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway
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Schisandrin B Inhibits LPS‐Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway
Schisandrin B Inhibits LPS‐Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway

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Schisandrin B Inhibits LPS‐Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway
Schisandrin B Inhibits LPS‐Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway
Journal Article

Schisandrin B Inhibits LPS‐Induced Endometritis Through Attenuating Ferroptosis via AMPK/PGC1α/Nrf2 Signalling Pathway

2024
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Overview
Endometritis is one of the common reproductive diseases in human and animal. In recent years, a number of studies have found that Schisandra B (Sch B), as a natural Chinese medicine extract, has antioxidant, anti‐inflammatory and other biological activities. Based on the above, in this study, mice were used to conduct an in vivo experiment to investigate the effect and mechanism of Sch B on lipopolysaccharide (LPS)‐induced endometritis. Haematoxylin and eosin (H&E) staining was used to detect the pathological changes of uterine tissue and western blot was used to detect the expression levels of signalling pathways and key genes for ferroptosis. The results showed that Sch B significantly inhibited the pathological injury of uterine tissue, myeloperoxidase (MPO) activity, the activation of NF‐κB pathway and the production of TNF‐α and IL‐1β. Furthermore, Sch B effectively inhibited ferroptosis by inhibiting malondialdehyde (MDA) and iron production and promoting the expression of ferroptosis suppressor genes GPX4 and ferritin. In conclusion, Sch B inhibited LPS‐induced endometritis through alleviating inflammatory response and ferroptosis via AMPK/PGC1α/Nrf2 signalling pathway.