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العنوان
Evaluation Of The Potential Teratogenic Effects Of Antidepressant Drug Desvenlafaxine On Pregnant Albino Rats And Their Embryos /
المؤلف
Ahmed, Sarah Hassan Ahmed Ahmed Sayed.
هيئة الاعداد
باحث / Sarah Hassan Ahmed Ahmed Sayed Ahmed
مشرف / Abd Elwahab Abo Bakr Mousa Elghareb
مشرف / Ali Hussein Abu Almaaty
مشرف / Heba Ali Abd El-Rahman
مناقش / Amoura Mohamed Abou-El-Naga
مناقش / Hala Mohamed Ebaid Ali
تاريخ النشر
2022.
عدد الصفحات
305 p. ;
اللغة
الإنجليزية
الدرجة
الدكتوراه
التخصص
Multidisciplinary تعددية التخصصات
تاريخ الإجازة
25/9/2022
مكان الإجازة
جامعة بورسعيد - كلية العلوم ببورسعيد - Zoology Department
الفهرس
Only 14 pages are availabe for public view

from 305

from 305

Abstract

Depression during pregnancy adversely affects fetal development. Desvenlafaxine is SNRI (Serotonin Norepinephrine Reuptake Inhibitor) that is taken orally and had several recorded clinical trials established its effectiveness for depression therapy and selected for being the antidepressant of choice for pregnant women who suffer from anxiety or depression. Concerns about its developmental safety have been raised. There isn’t a lot of information about desvenlafaxine’s safety during pregnancy. The present study aims to investigate the possible morphological, histopathological, biochemical, immunohistochemical, and gene expression effects of maternal and prenatal exposure to one of the antidepressants through maternal administration of desvenlafaxine in female Wistar rats during the gestation period. Thirty pregnant rats (Rattus norvegicus) weighing (180-200) were divided into three groups, with ten rats in each group. The control group was administered an oral dose of distilled water and the treated groups were administered two oral doses of desvenlafaxine (5.14 mg/kg and 10.28 mg/Kg) from the 5th day to the 19th day of gestation. At the end of the gestation period, the females were sacrificed. Desvenlafaxine administration affected the body weight gain in the mothers, the weight of the uterus in addition to unequal distribution of fetuses in the two uteri horns, increased post-implantation loss index, and decreased the number of corpora lutea. Moreover, desvenlafaxine caused growth retardation in the fetuses, as evidenced by a significant decrease in fetal body weight, fetal length, and tail length. It also induced many fetal abnormalities. Examination of the placenta, maternal and fetal liver, kidney, and brain of pregnant rats treated with desvenlafaxine showed several histopathological changes. The oxidative injury was noticed in the fetal liver as the level of lipid peroxidation Malondialdehyde (MDA) was remarkably elevated, while a severe reduction in glutathione (GSH), Catalase (CAT), and Superoxide Dismutase (SOD) was found. Immunohistochemical analysis of fetal rat livers showed that groups treated with desvenlafaxine demonstrated a significant increase of BAX and Caspase-3 protein immunoreactivity compared with that in the controls. Moreover, immunohistochemical analysis of maternal and fetal rat brains showed that groups treated with desvenlafaxine demonstrated a significant increase of NGF protein immunoreactivity compared with that in the controls. Gene expression results revealed upregulation of mRNA BDNF and S100B expression. It has been found that gestational usage of desvenlafaxine caused maternal and fetal risk. Desvenlafaxine should be used by pregnant women if its benefits are more than the potential risks.