Literature DB >> 23199550

Creation of a female rabbit model for intrauterine adhesions using mechanical and infectious injury.

Fang Liu1, Zhi-Jun Zhu, Peng Li, Yuan-Li He.   

Abstract

BACKGROUND: Intrauterine adhesions (IUA) are associated with secondary amenorrhea, infertility, and recurrent pregnancy loss. An IUA animal model would contribute to research on the pathogenesis and pathologic changes of IUA and the exploration of new treatments.
MATERIALS AND METHODS: Eighty female rabbits were randomly divided into five groups: mechanical injury (16), infectious injury (16), dual injury (16), experimental control (16), and normal (16). Three methods were applied to establish the model: uterine curettage, uterine cavity left alone, lipopolysaccharide surgical suture in place for 48 h, and suture retention for 48 h after curettage. A sterile surgical suture was left in the uterine cavity for 48 h in the experimental control group. Histologic changes were monitored at 0, 24, 48, and 72 h and 7, 14, and 28 d after operation.
RESULTS: The experiments revealed that endometrium injured by simple curettage or infection could be repaired. Although endometrial regeneration was severely impaired by dual injury, the ratio of the area with endometrial stromal fibrosis to total endometrial area significantly increased (P < 0.01), and the number of endometrial glands was significantly reduced (P < 0.01).
CONCLUSIONS: The method of dual injury can establish a stable rabbit IUA model.
Copyright © 2013 Elsevier Inc. All rights reserved.

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Year:  2012        PMID: 23199550     DOI: 10.1016/j.jss.2012.11.009

Source DB:  PubMed          Journal:  J Surg Res        ISSN: 0022-4804            Impact factor:   2.192


  13 in total

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7.  Quantification of the CM-Dil-labeled human umbilical cord mesenchymal stem cells migrated to the dual injured uterus in SD rat.

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8.  The role of KDR in intrauterine adhesions may involve the TGF-β1/Smads signaling pathway.

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10.  Foxf2 and Smad6 co-regulation of collagen 5A2 transcription is involved in the pathogenesis of intrauterine adhesion.

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