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Advanced Pharmaceutical Bulletin
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Article History
Submitted: 28 Apr 2014
Revised: 22 Jun 2014
First published online: 01 Jun 2015

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Adv Pharm Bull. 2015;5(2):195-199 doi: 10.15171/apb.2015.027
PMID:26236657        PMCID:PMC4517074

Ghrelin Administration Increases the Bax/Bcl-2 Gene Expression Ratio in the Heart of Chronic Hypoxic Rats

Original Research

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.





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