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February 25, 2026Antioxidants0 citationsOpen Access

Astragaloside IV Alleviates Trueperella pyogenes-Induced Endometritis via the Nrf2/HO-1 Signaling Pathway

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CGChunyang GouHMHetian MuYWYeqin Wang

Key Points

  • To investigate the therapeutic effects of Astragaloside IV on T. pyogenes-induced endometritis and understand the underlying mechanisms.
  • Utilized mouse uteri and goat endometrial epithelial cells to model T. pyogenes infection.
  • Applied histopathology, molecular biology, and transcriptomic technologies for analysis.
  • Examined the role of the Nrf2/HO-1 signaling pathway in mediating defense against inflammation and oxidative stress.
  • Astragaloside IV treatment significantly reduced endometrial damage caused by T. pyogenes.
  • The compound suppressed inflammation, apoptosis, and oxidative stress in infected tissues.
  • Activation of the Nrf2/HO-1 pathway was confirmed, while Nrf2 inhibition negated protective effects.

Abstract

The increasing antimicrobial resistance of T. pyogenes, one of the principal pathogens associated with endometritis, presents a formidable challenge in veterinary medicine. Astragaloside IV (AS-IV) is a triterpene saponin compound isolated from the traditional Chinese medicine Astragalus membranaceus. While recognized as the primary bioactive constituent of Astragalus membranaceus with diverse pharmacological properties, its potential to counteract T. pyogenes-induced endometritis has yet to be elucidated. In the current study, T. pyogenes infection models were successfully established in both mouse uteri and cultured goat endometrial epithelial cells (gEECs). Integrating histopathology, molecular biology and transcriptomic technology, this study characterized the multifaceted biological effects of AS-IV. Transcriptomic analysis indicates that the regulatory effects of AS-IV on T. pyogenes-induced infection are primarily associated with the enrichment of signaling pathways related to inflammation, apoptosis, and oxidative stress. Subsequent validation demonstrated that AS-IV treatment effectively alleviated T. pyogenes-induced endometrial damage by suppressing inflammation, apoptosis, and oxidative stress. These effects were mediated through Nrf2 and its downstream target HO-1, a mechanism further confirmed by the loss of protection upon Nrf2 inhibition. In summary, AS-IV protects the endometrium against T. pyogenes-induced inflammatory and oxidative damage by activating the Nrf2/HO-1 signaling pathway.

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Cite This Study

Gou et al. (2026) studied this question.

synapsesocial.com/papers/699e9143f5123be5ed04ea00https://doi.org/10.3390/antiox15020271
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