Open AccessMaternal separation can affect the reproductive system by inflammasome activation in female mice
Author(s) -
Kajal Khodamoradi,
Hossein Amini-Khoei,
Zahra Khosravizadeh,
Seyed Reza Hosseini,
Ahmad Reza Dehpour,
Gholamreza Hassanzadeh
Publication year - 2019
Publication title -
journal of contemporary medical sciences
Language(s) - English
Resource type - Journals
eISSN - 2415-1629
pISSN - 2413-0516
DOI - 10.22317/jcms.v5i3.601
Subject(s) - apoptosis , inflammasome , andrology , immunocytochemistry , endocrinology , tlr4 , medicine , tumor necrosis factor alpha , biology , inflammation , chemistry , biochemistry
Objective: The aim of this study is to investigate effect of maternal separation stress on the ovarian function in adult female mice.
Methods: In this study, maternal separation in pups was performed during post-natal days (PND) 2 to 14. The histological alterations in ovarian tissue, ROS production (using DCFH-DA assay), gene expression of NLRP3, ASC, caspase-1, TLR4, BAX, BCL-2 and TNFα (using RT-PCR), protein levels of ATP, GPx, IL-1β and IL-18 (using ELISA). Also, protein expression of caspase-3 and NLRP3 (using immunocytochemistry) were evaluated.
Results: Results showed that maternal separation decreased percentage of primordial follicles while increased percentage of secondary and graafian follicles. In addition, maternal separation increased ROS production and decreased ATP and GPx concentrations. Furthermore, maternal separation significantly affected expression of cytokines and genes involved in inflammation and apoptosis including NLRP3, ASC, caspase-1, TLR4, TNFα, IL-1β, IL-18 BAX and BCL2. Findings also showed that stress-induced maternal separation significantly increased percentage of caspase-3 and NLRP3 positive cells. We concluded that maternal separation stress has harmful effects on ovarian tissue.
Conclusion: It seems that these harmful effects are probably occur through increase of ROS production and impact on mitochondrial function, inflammatory process and apoptosis pathways.