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<span style="font-size:15.0pt;mso-bidi-font-family: "Times New Roman"" lang="EN-US">Increased cardiac endothelin-1 and nitric oxide in adriamycin-induced acute cardiotoxicity: Protective effect of <i>Ginkgo biloba</i> extract </span>

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Title Increased cardiac endothelin-1 and nitric oxide in adriamycin-induced acute cardiotoxicity: Protective effect of Ginkgo biloba extract
 
Creator El-Boghdady, Noha Ahmed
 
Subject Adriamycin
Endothelin-1
Ginkgo biloba extract
Cardiotoxicity
Nitric oxide
Tumor necrosis factor-α
 
Description 202-209
Cardiotoxicity and congestive heart failure are
the major factors that limit the use of anti-neoplastic drug adriamycin (ADR).
There is increasing experimental evidence that endothelin-1 (ET-1) and nitric
oxide (NO) are vasoactive mediators that regulate cardiac performance. The
present study was undertaken to investigate the role of ET-1 and NO in
ADR-induced acute cardiotoxicity and to evaluate the protective effect of Ginkgo
biloba extract (EGb761) in rats. A single dose of ADR (20 mg/kg i.p.)
caused a significant increase in the cardiac enzyme activities of aspartate
transaminases (AST), lactate dehydrogenase (LDH) and creatine phosphokinase
isoenzyme (CK-MB) in the serum of animals. This was accompanied by significant
increase in cardiac malondialdehyde (MDA), total antioxidant capacity (TAC),
tumor necrosis factor-alpha (TNF-α), ET-1 and nitrite/nitrate (NOx) levels. On
the other hand, reduced glutathione (GSH) was significantly depressed.
Histopathological examination of heart tissues showed hyalinization of the
myocardium, with interstitial edema and inflammatory exudates. Pre-treatment of
the animals with EGb761 (100 mg/kg, orally) 10 days before and 5 days after ADR
treatment reversed the cardiac enzyme levels to normal value, decreased cardiac
MDA, TAC, TNF-α, ET-1 and NOx, increased GSH and reversed the histopathological
damage induced by ADR. In conclusion, the cardioprotective effects of EGb761 on
markers of ADR-induced acute cardiotoxicity appeared to have been mediated by
the regulation of inflammatory and vasoactive mediators, as well as the
inhibition of membrane lipid peroxidation. Thus, EGb761 may find use as
promising adjuvant therapy to ameliorate cardiotoxicity of ADR.
 
Date 2013-06-04T13:00:16Z
2013-06-04T13:00:16Z
2013-06
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/18690
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJBB Vol.50(3) [June 2013]