Elevated NF-κB signaling in Asherman syndrome patients and animal models
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Xiangzhen Wang1,2, Nana Ma3, Qiannan Sun4, Chenlingzi Huang1, Yanmei Liu5, Xin Luo1
1The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China, 510630
2Nanshan Maternity and Child Healthcare Hospital of Shenzhen, Shenzhen, Guangdong, China, 518052
3The First Affiliated Hospital of Xinxiang medical college of Henan, Xinxiang, Henan, China, 453100
4Changzhi City People’s Hospital of Shanxin Medical University Affiliated Hospital, Changzhi, Shanxi, China, 046000
5Huadu District, Guangzhou City People’s Hospital, Guangzhou, Guangdong, China, 510630
Xiangzhen Wang, email: email@example.com
Xin Luo, email: firstname.lastname@example.org
Keywords: NF-κB, Asherman syndrome, intrauterine adhesion, pregnancy, uterine disease
Received: October 09, 2016 Accepted: January 09, 2017 Published: January 27, 2017
Asherman syndrome (intrauterine adhesion) is often associated with menstrual abnormalities, infertility and recurrent miscarriage in female. Currently the molecular mechanism regulating the pathogenesis of Asherman syndrome is not known. Here we revealed that the inflammatory factor NF-κB expression is significantly elevated in the endometrial samples of Asherman syndrome patients. To further study the molecular mechanisms, we established an Asherman syndrome rat model and confirmed the important role of NF-κB in the pathogenesis of Asherman syndrome. In addition, our rat model provided direct evidence that intrauterine adhesion results in impaired pregnancy, supporting the clinical association between intrauterine adhesion and mis-regulated pregnancy. Our result identified NF-κB as a novel pathogenesis factor of Asherman syndrome and provided new insights for the prevention and treatment of intrauterine adhesions in Asherman syndrome patients.
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