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Advanced Pharmaceutical Bulletin
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Article History
Submitted: 12 Sep 2015
Revised: 18 Feb 2016
Accepted: 22 Feb 2016
First published online: 17 Mar 2016

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Adv Pharm Bull. 2016;6(1):99-103 doi: 10.15171/apb.2016.015
PMID:27123424        PMCID:PMC4845552

Alteration in Inflammation-related miR-146a Expression in NF-KB Signaling Pathway in Diabetic Rat Hippocampus

Original Research

Fatemeh Habibi 1, Farhad Ghadiri Soufi 2, Rafighe Ghiasi 3, Amir Mahdi Khamaneh 4, Mohammad Reza Alipour 1 *

1 Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
2 Molecular Medicine Research Center, Hormozgan University of Medical Sciences, Bandar Abbas, Iran.
3 Department of Physiology, Tabriz University of Medical Sciences, Tabriz, Iran.
4 School of Advanced Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran.



Abstract
Purpose: The purpose of the present study is to evaluate the expression of miR-146a gene, its adaptor genes (TRAF6, NF-KB, and IRAK1), and possible changes in the cellular signaling pathway in diabetic hippocampus tissue. Methods: Male Sprague–Dawley rats are randomly selected and divided into control and diabetic (n=6) groups. Diabetes induced by the single-dose injection of nicotinamide [110 mg/kg, (i.p.)], 15 min before streptozotocin (50 mg/kg; i.p.) in 12-h fasted rats. The rats are kept at the laboratory for two months. After anaesthetization, hippocampus of the rats was removed in order to measure the expression of miR-146a, NFK-B, IRAK1, and TRAF6 genes using real-time PCR and activity of NF-KB as well as amount of apoptosis rate using ELISA. Results: The results indicated a reduction in expression of miR-146a and an increase in expression of IRAK1, NF-KB, and TRAF6 genes in the hippocampus of diabetic rats compared to control. Also it reveals an increase in the activity of NF-KB and apoptosis rate in the hippocampus of diabetic rats. Conclusion: Our results report the probability that reduction of miR-146a expression in the negative feedback loop between miR-146a and NF-KB increases NF-kB expression and thus intensifies inflammation and apoptosis in hippocampus.





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