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.