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Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice
Gestational diabetes is defined as carbohydrate intolerance with onset or first recognition during pregnancy. Diabetes during pregnancy increases the incidences of congenital anomalies, in a mother and her embryo. Oxidative stress has been implicated to be responsible in diabetic embryopathy. In this...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Shaheed Beheshti University of Medical Sciences
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6094439/ https://www.ncbi.nlm.nih.gov/pubmed/30127819 |
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author | Vafaei-Pour, Zeinab Shokrzadeh, Mohammad Jahani, Monireh Shaki, Fatemeh |
author_facet | Vafaei-Pour, Zeinab Shokrzadeh, Mohammad Jahani, Monireh Shaki, Fatemeh |
author_sort | Vafaei-Pour, Zeinab |
collection | PubMed |
description | Gestational diabetes is defined as carbohydrate intolerance with onset or first recognition during pregnancy. Diabetes during pregnancy increases the incidences of congenital anomalies, in a mother and her embryo. Oxidative stress has been implicated to be responsible in diabetic embryopathy. In this study, we used nanoceria as an antioxidant for amelioration of diabetic embryopathy in diabetic mice. The female mice were divided into 5 groups (6 mice per group). Diabetes was induced by a single dose of streptozotocin (60 mg/kg IP) that dissolved in citrate buffer (pH = 4.6). Blood glucose was checked in 0,5,10, and 15 days of pregnancy. The diabetic state was confirmed when the blood glucose concentration exceeded 200 mg/dL. On the day 16 of pregnancy, all animals were anesthetized with ether and embryos were excised; then oxidative stress, pathological parameters, number of implantations, miscarriage, and live embryo were assayed. Histological study showed that diabetes induced abortion; decrease in weight of mothers, embryo, and the number of embryos were observed. In diabetic mice, significant increase in lipid peroxidation (LPO), ROS formation, and protein carbonyl content were observed. Glutathione (GSH) concentration is found to be decreased in embryo tissue in diabetic mice. Nanoceria treatment significantly inhibited embryonic oxidative stress and also pathologic changes in diabetic mice. Our research showed that diabetes act as a teratogen agent for fetal development and nanoceria abrogated diabetes induced embryopathy via its antioxidant effects. So, early detection of diabetes in pregnancy and antioxidant administration can attenuate these complications. |
format | Online Article Text |
id | pubmed-6094439 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Shaheed Beheshti University of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-60944392018-08-20 Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice Vafaei-Pour, Zeinab Shokrzadeh, Mohammad Jahani, Monireh Shaki, Fatemeh Iran J Pharm Res Original Article Gestational diabetes is defined as carbohydrate intolerance with onset or first recognition during pregnancy. Diabetes during pregnancy increases the incidences of congenital anomalies, in a mother and her embryo. Oxidative stress has been implicated to be responsible in diabetic embryopathy. In this study, we used nanoceria as an antioxidant for amelioration of diabetic embryopathy in diabetic mice. The female mice were divided into 5 groups (6 mice per group). Diabetes was induced by a single dose of streptozotocin (60 mg/kg IP) that dissolved in citrate buffer (pH = 4.6). Blood glucose was checked in 0,5,10, and 15 days of pregnancy. The diabetic state was confirmed when the blood glucose concentration exceeded 200 mg/dL. On the day 16 of pregnancy, all animals were anesthetized with ether and embryos were excised; then oxidative stress, pathological parameters, number of implantations, miscarriage, and live embryo were assayed. Histological study showed that diabetes induced abortion; decrease in weight of mothers, embryo, and the number of embryos were observed. In diabetic mice, significant increase in lipid peroxidation (LPO), ROS formation, and protein carbonyl content were observed. Glutathione (GSH) concentration is found to be decreased in embryo tissue in diabetic mice. Nanoceria treatment significantly inhibited embryonic oxidative stress and also pathologic changes in diabetic mice. Our research showed that diabetes act as a teratogen agent for fetal development and nanoceria abrogated diabetes induced embryopathy via its antioxidant effects. So, early detection of diabetes in pregnancy and antioxidant administration can attenuate these complications. Shaheed Beheshti University of Medical Sciences 2018 /pmc/articles/PMC6094439/ /pubmed/30127819 Text en This is an Open Access article distributed under the terms of the Creative Commons Attribution License, (http://creativecommons.org/licenses/by/3.0/) which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Vafaei-Pour, Zeinab Shokrzadeh, Mohammad Jahani, Monireh Shaki, Fatemeh Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice |
title | Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice |
title_full | Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice |
title_fullStr | Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice |
title_full_unstemmed | Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice |
title_short | Embryo-Protective Effects of Cerium Oxide Nanoparticles against Gestational Diabetes in Mice |
title_sort | embryo-protective effects of cerium oxide nanoparticles against gestational diabetes in mice |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6094439/ https://www.ncbi.nlm.nih.gov/pubmed/30127819 |
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