Journal of Stress Physiology &
Biochemistry, Vol. 9 No. 1
2013, pp. 273-282 ISSN 1997-0838
Original Text Copyright (cc) 2013 by Kheyabany,
Nabavizadeh, Vaezi, Alizadeh, Nahrevanian, Moslehi and Azizian
ORIGINAL
ARTICLE
Data source : Google Scholar
QueryDate : 2016-12-24
Cites : 2
Protective Effect of Ghrelin
on Isoniazid-induced Liver Injury in Rat
Shadi Sar Kheyr Kheyabany1,
Fatemeh Nabavizadeh2*, Gholam Hassan Vaezi3, Ali
Mohammad Alizadeh4, Hossein Nahrevanian5, Azam
Moslehi2, Saleh Azizian4 1 Department of biology, Damghan Branch, Islamic Azad
University, Damghan, Iran 2 Department of physiology, Tehran University of Medicale
Sciences and Health Services, Tehran, Iran 3 Department of biology, Islamic Azad University, Damghan
Branch, Semnan, Iran 4 Cancer Research Center, Tehran University of medical
sciences, Tehran, Iran. 5 Department of Parasitoligy, Pasteur Institute of Iran,
Tehran 13164, Iran
*E-Mail: nabavizadeh2000@yahoo.com
Received October 30, 2012
Ghrelin (GHR) is a
peptide that has protective effects on many tissues injury. It has
anti-inflammatory and anti-oxidant effects. Isoniazid (INH) a widely
used antituberculosis drug, has hepatotoxic side effect. The aim of
this study was to evaluate the protective role of ghrelin in liver
toxicity due to isoniazid. Eighteen male rats were used in this study
and divided in to three groups. Including: control, isoniazid,
isoniazid and ghrelin groups. Nitric oxide (NO), prostaglandin E2
(PGE2), and hepatic enzymes, ALT (alanine aminotransferase), AST
(aspartate aminotransferase), ALK(alkaline phosphatas), were assessed
and histologic study of liver were performed as indicators of liver
damage following isoniazid toxicity. Ghrelin significantly increased NO
metabolites and decreased PGE2 level comparison with INH group, but had
no significant change compared to the control group. This study
showed that ghrelin administration inhibited liver injury in rats due
to isoniazid toxicity. The liver protective role of ghrelin may be
mediated at least in part by its anti-inflammatory effect.
