Ovariectomy with simulated vaginal delivery to establish a rat model for pelvic organ prolapse.

IF 2.8 4区 医学 Q3 CELL BIOLOGY
Tao Guo, Zhe Du, Xiu-Qi Wang, Jing-He Lang, Zhi-Jing Sun
{"title":"Ovariectomy with simulated vaginal delivery to establish a rat model for pelvic organ prolapse.","authors":"Tao Guo,&nbsp;Zhe Du,&nbsp;Xiu-Qi Wang,&nbsp;Jing-He Lang,&nbsp;Zhi-Jing Sun","doi":"10.1080/03008207.2023.2199091","DOIUrl":null,"url":null,"abstract":"<p><p>The widespread prevalence of Pelvic Organ Prolapse (POP) and the paucity of ongoing treatments prompted us to develop a unique rat model combining ovariectomy and simulated vaginal delivery. We hypothesized that the tissue changes caused by low hormone levels and mechanical stretch could complement each other. Thus, the combined model can potentially mimic the collagen metabolism of vaginal wall tissue as well as mechanical stretch properties to complement disease progression in POP. Ovariectomy with sequential simulated vaginal delivery was performed on rats in the modeling group. Sham surgeries were performed as control. At 2, 4, and 12 weeks after modeling, the vaginal tissues of rats were evaluated by Masson's trichrome staining, Picro-Sirius red staining, immunohistochemistry, western blotting, and uniaxial tensile tests. Compared to the control group, the vaginal tissues of the model rats showed an atrophic epithelial layer and loose collagen fibers. The smooth muscle fibers were ruptured, smaller in diameter, and disorganized. The ratio of collagen type I/III significantly increased, but the contents of both Collagen I and III decreased. The expression of metalloproteinases 2 and 9 in the tissues increased, and the expression of tissue inhibitors of metalloproteinases 1 and 2 decreased. The tangent modulus of the tissues was significantly increased in the model rats. We verified a novel method to establish a pelvic organ prolapse model in rats. This approach combined the advantages of low hormone levels and mechanical stretch effects.</p>","PeriodicalId":10661,"journal":{"name":"Connective Tissue Research","volume":null,"pages":null},"PeriodicalIF":2.8000,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Connective Tissue Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/03008207.2023.2199091","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

The widespread prevalence of Pelvic Organ Prolapse (POP) and the paucity of ongoing treatments prompted us to develop a unique rat model combining ovariectomy and simulated vaginal delivery. We hypothesized that the tissue changes caused by low hormone levels and mechanical stretch could complement each other. Thus, the combined model can potentially mimic the collagen metabolism of vaginal wall tissue as well as mechanical stretch properties to complement disease progression in POP. Ovariectomy with sequential simulated vaginal delivery was performed on rats in the modeling group. Sham surgeries were performed as control. At 2, 4, and 12 weeks after modeling, the vaginal tissues of rats were evaluated by Masson's trichrome staining, Picro-Sirius red staining, immunohistochemistry, western blotting, and uniaxial tensile tests. Compared to the control group, the vaginal tissues of the model rats showed an atrophic epithelial layer and loose collagen fibers. The smooth muscle fibers were ruptured, smaller in diameter, and disorganized. The ratio of collagen type I/III significantly increased, but the contents of both Collagen I and III decreased. The expression of metalloproteinases 2 and 9 in the tissues increased, and the expression of tissue inhibitors of metalloproteinases 1 and 2 decreased. The tangent modulus of the tissues was significantly increased in the model rats. We verified a novel method to establish a pelvic organ prolapse model in rats. This approach combined the advantages of low hormone levels and mechanical stretch effects.

卵巢切除模拟阴道分娩建立大鼠盆腔器官脱垂模型。
盆腔器官脱垂(POP)的广泛流行和持续治疗的缺乏促使我们开发了一种独特的大鼠模型,结合卵巢切除术和模拟阴道分娩。我们假设低激素水平引起的组织变化和机械拉伸可以互补。因此,联合模型可以潜在地模拟阴道壁组织的胶原代谢以及机械拉伸特性,以补充POP的疾病进展。造模组大鼠进行卵巢切除术并连续模拟阴道分娩。假手术作为对照组。造模后2、4、12周,采用马松三色染色、小天狼星红染色、免疫组织化学、免疫印迹和单轴拉伸试验对大鼠阴道组织进行评价。与对照组相比,模型大鼠阴道组织上皮层萎缩,胶原纤维疏松。平滑肌纤维断裂,直径变小,组织紊乱。I型胶原/III型胶原比例显著升高,但I型和III型胶原含量均降低。组织中金属蛋白酶2和9的表达增加,金属蛋白酶1和2的组织抑制剂表达减少。模型大鼠组织的切线模量明显增加。我们验证了一种建立大鼠盆腔器官脱垂模型的新方法。这种方法结合了低激素水平和机械拉伸效应的优点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Connective Tissue Research
Connective Tissue Research 生物-细胞生物学
CiteScore
6.60
自引率
3.40%
发文量
37
审稿时长
2 months
期刊介绍: The aim of Connective Tissue Research is to present original and significant research in all basic areas of connective tissue and matrix biology. The journal also provides topical reviews and, on occasion, the proceedings of conferences in areas of special interest at which original work is presented. The journal supports an interdisciplinary approach; we present a variety of perspectives from different disciplines, including Biochemistry Cell and Molecular Biology Immunology Structural Biology Biophysics Biomechanics Regenerative Medicine The interests of the Editorial Board are to understand, mechanistically, the structure-function relationships in connective tissue extracellular matrix, and its associated cells, through interpretation of sophisticated experimentation using state-of-the-art technologies that include molecular genetics, imaging, immunology, biomechanics and tissue engineering.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信