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Role of Oxytocin in deceleration of early atherosclerotic inflammatory processes in adult male rats

مؤلف البحث
Marwa A. Ahmed, Gehan M. ELosaily
مجلة البحث
Int J Clin Exp Med
المشارك في البحث
الناشر
www.ijcem.com
تصنيف البحث
1
عدد البحث
4(3)
موقع البحث
www.ijcem.com
سنة البحث
2011
صفحات البحث
169-178
ملخص البحث

Abstract: Objective: The study aimed to examine the effect of exogenous OT administration on the inflammation and
atherosclerosis in adult male rats and its possible mechanisms. Thirty adult male rats equally divided into three
groups. Control group fed regular diet; group II fed control diet supplemented with L-methionine for 10 weeks. Group
III received L-methionine and oxytocin treatment for 10 weeks. RT-PCR analysis showed that OT administration increased
oxytocin receptor mRNA (2 fold, P, 0.05). Blood samples were evaluated for total homocysteine, interlukin-6
(IL-6), monocyte chemoatrratant protein-1 (MCP-1) and C-reactive protein (CRP) by ELIZA. lipid profile, nitric oxide
(NO), malondialdehyde (MDA) and reduced glutathione (GSH) were determined. Specimens from aorta were processed
for immunohistochemical staining for Aorta nuclear factor _B (NF-κB) p65 protein. Result showed that OT administration
to group III decreased the plasma levels IL-6, MCP-1and CRP levels which were elevated in group II.
Moreover, there was decrease of the oxidative stress of group III in terms of increased plasma levels of NO and GSH
and decreased plasma levels of MDA in blood. In addition, rats of group II showed histological abnormalities manifested
by thickening and ulceration of the aortic wall. Marked increased expression of NF-κB in aorta of in group II
was detected. However, OT administration restores the histological structure of the aorta and decreased the expression
of NF-κB in aorta of group III similar to the control group. Conclusion: OT has anti inflammatory pathway in
atherosclerosis as it decelerates atherosclerosis by decreasing the proinflammatory responses through many mechanisms,
mainly the up regulation of its receptors.