Mohammad Reza Aliparasti
1, Mohammad Reza Alipour
1, Shohreh Almasi
2, Hadi Feizi
3*1 Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
2 Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
3 Department of Physiology, Zanjan University of Medical Sciences, Zanjan, Iran.
Abstract
Purpose:
Programmed cell death or apoptosis, is a
biochemical procedure that initiates due to some conditions, including hypoxia.
Bax and Bcl-2 are among the agents that regulate apoptosis. The amplification
of the first one triggers the initiation of apoptosis, and the second one
prevents it. Ghrelin is an endogenous peptide that antiapoptosis is its new
effect. The aim of this study is to examine the effect of ghrelin on the
Bax/Bcl-2 ratio.
Methods:
Twenty four wistar rats were divided randomly
in three groups; control, hypoxic + saline and hypoxic + ghrelin. Hypoxic
animals lived in O2 11% for 2 weeks and received either saline or ghrelin
subcutaneously daily. The bax and Bcl-2 gene expression were measured by
Real-Time RT-PCR.
Results:
Chronic hypoxia increased the Bax gene
expression significantly compared with normal animals (P = 0.008), but
the Bcl-2 was not affected by hypoxia. The Bax/Bcl-2 ratio also amplified
significantly (P=0.005). Ghrelin administration
significantly increased the Bax/Bcl-2 ratio in the hypoxic
animals compared to the hypoxic + saline and normal groups
(p=0.042 and P= 0.001,
respectively).
Conclusion: In the present study, animals’ treatment with ghrelin leads to an
increment of Bax/Bcl-2 ratio, which indicates a controversy related to
cardioprotection of ghrelin.