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Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model

Premature ovarian failure (POF) is one of the most common causes of infertility in women. In our present study, we established cyclophosphamide- (CTX-) induced POF rat model and elucidated its effect on ovarian function. We detected the serum estrogen, follicle stimulating hormone, and anti-Mülleria...

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Autores principales: Song, Dan, Zhong, Yun, Qian, Chunfeng, Zou, Qinyan, Ou, Jian, Shi, Yichao, Gao, Liang, Wang, Gaigai, Liu, Zhenxing, Li, Haibo, Ding, Hailei, Wu, Huihua, Wang, Fuxin, Wang, Jing, Li, Hong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4800076/
https://www.ncbi.nlm.nih.gov/pubmed/27047962
http://dx.doi.org/10.1155/2016/2517514
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author Song, Dan
Zhong, Yun
Qian, Chunfeng
Zou, Qinyan
Ou, Jian
Shi, Yichao
Gao, Liang
Wang, Gaigai
Liu, Zhenxing
Li, Haibo
Ding, Hailei
Wu, Huihua
Wang, Fuxin
Wang, Jing
Li, Hong
author_facet Song, Dan
Zhong, Yun
Qian, Chunfeng
Zou, Qinyan
Ou, Jian
Shi, Yichao
Gao, Liang
Wang, Gaigai
Liu, Zhenxing
Li, Haibo
Ding, Hailei
Wu, Huihua
Wang, Fuxin
Wang, Jing
Li, Hong
author_sort Song, Dan
collection PubMed
description Premature ovarian failure (POF) is one of the most common causes of infertility in women. In our present study, we established cyclophosphamide- (CTX-) induced POF rat model and elucidated its effect on ovarian function. We detected the serum estrogen, follicle stimulating hormone, and anti-Müllerian hormone of mice models by ELISA and evaluated their folliculogenesis by histopathology examination. Our study revealed that CTX administration could severely disturb hormone secretion and influence folliculogenesis in rat. This study also detected ovarian cells apoptosis by deoxy-UTP-digoxigenin nick end labeling (TUNEL) and demonstrated marked ovarian cells apoptosis in rat models following CTX administration. In order to explore the potential of human umbilical cord mesenchymal stem cells (UCMSCs) in POF treatment, the above indexes were used to evaluate ovarian function. We found that human UCMSCs transplantation recovered disturbed hormone secretion and folliculogenesis in POF rat, in addition to reduced ovarian cell apoptosis. We also tracked transplanted UCMSCs in ovaries by fluorescence in situ hybridization (FISH). The results manifested that the transplanted human UCMSCs could reside in ovarian tissues and could survive for a comparatively long time without obvious proliferation. Our present study provides new insights into the great clinical potential of human UCMSCs in POF treatment.
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spelling pubmed-48000762016-04-04 Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model Song, Dan Zhong, Yun Qian, Chunfeng Zou, Qinyan Ou, Jian Shi, Yichao Gao, Liang Wang, Gaigai Liu, Zhenxing Li, Haibo Ding, Hailei Wu, Huihua Wang, Fuxin Wang, Jing Li, Hong Biomed Res Int Research Article Premature ovarian failure (POF) is one of the most common causes of infertility in women. In our present study, we established cyclophosphamide- (CTX-) induced POF rat model and elucidated its effect on ovarian function. We detected the serum estrogen, follicle stimulating hormone, and anti-Müllerian hormone of mice models by ELISA and evaluated their folliculogenesis by histopathology examination. Our study revealed that CTX administration could severely disturb hormone secretion and influence folliculogenesis in rat. This study also detected ovarian cells apoptosis by deoxy-UTP-digoxigenin nick end labeling (TUNEL) and demonstrated marked ovarian cells apoptosis in rat models following CTX administration. In order to explore the potential of human umbilical cord mesenchymal stem cells (UCMSCs) in POF treatment, the above indexes were used to evaluate ovarian function. We found that human UCMSCs transplantation recovered disturbed hormone secretion and folliculogenesis in POF rat, in addition to reduced ovarian cell apoptosis. We also tracked transplanted UCMSCs in ovaries by fluorescence in situ hybridization (FISH). The results manifested that the transplanted human UCMSCs could reside in ovarian tissues and could survive for a comparatively long time without obvious proliferation. Our present study provides new insights into the great clinical potential of human UCMSCs in POF treatment. Hindawi Publishing Corporation 2016 2016-03-07 /pmc/articles/PMC4800076/ /pubmed/27047962 http://dx.doi.org/10.1155/2016/2517514 Text en Copyright © 2016 Dan Song et al. https://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Song, Dan
Zhong, Yun
Qian, Chunfeng
Zou, Qinyan
Ou, Jian
Shi, Yichao
Gao, Liang
Wang, Gaigai
Liu, Zhenxing
Li, Haibo
Ding, Hailei
Wu, Huihua
Wang, Fuxin
Wang, Jing
Li, Hong
Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model
title Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model
title_full Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model
title_fullStr Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model
title_full_unstemmed Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model
title_short Human Umbilical Cord Mesenchymal Stem Cells Therapy in Cyclophosphamide-Induced Premature Ovarian Failure Rat Model
title_sort human umbilical cord mesenchymal stem cells therapy in cyclophosphamide-induced premature ovarian failure rat model
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4800076/
https://www.ncbi.nlm.nih.gov/pubmed/27047962
http://dx.doi.org/10.1155/2016/2517514
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