期刊
ANIMALS
卷 13, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/ani13071135
关键词
embryo; endotoxin; infertility; inflammatory; LPS
This study investigates the effects of lipopolysaccharide (LPS) endotoxin exposure on early embryonic development and fetal development in mice. It is found that LPS exposure leads to increased expression of Il-1 beta and Il-6, and significantly decreases the embryonic developmental rate. Different concentrations of LPS also have varying effects on placental weight, fetal weight, and crown-rump length (CRL). These findings suggest that LPS exposure during fertilization can result in abnormal embryonic phenotypes and fetal development, with potential long-term effects on epigenetic inheritance.
Simple Summary: The long-term effect of exposure to lipopolysaccharide (LPS) endotoxins during fertilization in mammals has not been clarified. In this study, we examined the influence of LPS on early embryonic development and fetal development in mice. The uteruses of mice were examined for the expression of genes related to the inflammatory response. The expression of Il-1 beta and Il-6 increased following the administration of 200 and 1000 mu g/kg LPS. Exposure to LPS during in vitro fertilization (IVF) significantly decreased the embryonic developmental rate. A concentration of 100 mu g/kg LPS significantly increased the placental weight and fetal crown-rump length (CRL), whereas a concentration of 200 mu g/kg LPS significantly decreased the placenta weight and fetal weight in vivo at 18.5 days post-coitus (dpc). In summary, this study demonstrated that LPS exposure during fertilization causes abnormal embryonic phenotypes and fetal development in mice. Maternal endotoxins may affect epigenetic inheritance in embryonic development from the early to late stages of pregnancy. Intrauterine inflammation can cause infertility by disrupting reproductive function. The pathogenesis underlying this process may primarily involve endotoxins from lipopolysaccharides (LPS), which are produced by Gram-negative bacteria. However, the long-term effects of endotoxins in mammalian pregnancy following LPS exposure during fertilization have not been clarified. In this study, we performed experiments to analyze the influence of LPS on early embryonic development and fetal development in mice. Mice uteruses were examined for the expression of genes related to the inflammatory response. The expression of Il-1 beta and Il-6 increased following the administration of 200 and 1000 mu g/kg LPS. Exposure to LPS using in vitro fertilization (IVF) significantly decreased the embryonic developmental rate. A concentration of 100 mu g/kg LPS significantly increased the placental weight and fetal crown-rump length (CRL), whereas a concentration of 200 mu g/kg LPS significantly decreased the placenta weight and fetal weight in vivo. These findings indicate that maternal LPS during fertilization affects fetal development until the late stage of pregnancy. Thus, maternal endotoxins may affect epigenetic inheritance during embryonic development from the early to late stages of pregnancy.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据