Ghrelin Administration Increases the Bax/Bcl-2 Gene Expression Ratio in the Heart of Chronic Hypoxic Rats
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. Gh...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Tabriz University of Medical Sciences
2015-06-01
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| Series: | Advanced Pharmaceutical Bulletin |
| Subjects: | |
| Online Access: | http://journals.tbzmed.ac.ir/APB/Abstract/APB_1745_20140428184508 |
| Summary: | 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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| ISSN: | 2228-5881 2251-7308 |