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Title: Notch Signaling in Intrauterine Growth Restriction in Rats: Is There a Modulatory Role for Melatonin?
Authors: Wafa Matar Alfadhli 
Supervisor: Prof. Maie Dawoud Al-Bader
Degree Awarded: Master's Degree in: Physiology
Keywords: Placenta ; Dexamethasone : IUGR : Melatonin : Notch
Issue Date: 2019
Publisher:  Kuwait university - college of graduate studies
Abstract: Notch signaling is involved in cell proliferation, differentiation and cell death. Recent research indicates that there is an important role for Notch proteins in normal fetal development and placental functions. However, molecular mechanisms that regulate the Notch signaling pathway during placental growth remain largely obscure. Melatonin, a hormone and an antioxidant, has neuroprotective and cardioprotective effects on offspring in pregnancies complicated by IUGR. We hypothesize that melatonin can reverse the effect of DEX and prevent IUGR. Since Notch signaling pathway is highly involved in placental development and function, we hypothesize that the expression of Notch receptors and its signaling pathway is affected in IUGR and this effect is reversed with melatonin administration. Pregnant Sprague-Dawley rats were divided into four groups: normal saline/control (C), normal saline and melatonin (MEL), DEX, DEX and melatonin (DEX+MEL) groups. Pregnant rats received daily intra-peritoneal (i.p.) injections of dexamethasone (DEX, DEX+MEL groups; 0.2 mg/kg) or saline (C, MEL group) from 15 days gestation (dg) up to day 18 or 20 dg. In the melatonin-treatment groups, rats received 0.01% melatonin in drinking water during their entire pregnancy until sacrifice. Serum melatonin level was estimated using ELISA. The Notch signaling component genes and proteins were estimated by PCR array and Western blotting, respectively in the labyrinth (LZ) and basal (BZ) zones of the placenta. There was no difference in serum melatonin level among groups. In LZ DII3, ADAM10 were significantly up-regulated in DEX group. In BZ, Notch 2, ADAM17, Ncstn, Psen 1 were significantly up-regulated in DEX group. In contrast, in melatonin group, Notch1, 2, ADAM10, ADAM17, ncstn were significantly down-regulated. IUGR is associated with changes in Notch pathway activity at the molecular level. Melatonin did not show any protective role against DEX regarding saving the fetal body weight nor the placental weight. Our results also showed that melatonin treatment modulates the activity of Notch pathway compared to the control group.
Appears in Programs:0530 Physiology (M.Sc.)

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