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Protective Effects of Houttuynia cordata Thunb. on Gentamicin-induced Oxidative Stress and Nephrotoxicity in Rats

Development of a therapy providing protection from, or reversing gentamicin-sulfate (GS)-induced oxidative stress and nephrotoxicity would be of great clinical significance. The present study was designed to investigate the protective effects of Houttuynia cordata Thunb. (HC) against gentamicin sulf...

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Autores principales: Kang, Changgeun, Lee, Hyungkyoung, Hah, Do-Yun, Heo, Jung Ho, Kim, Chung Hui, Kim, Euikyung, Kim, Jong Shu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Toxicology 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834437/
https://www.ncbi.nlm.nih.gov/pubmed/24278630
http://dx.doi.org/10.5487/TR.2013.29.1.061
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author Kang, Changgeun
Lee, Hyungkyoung
Hah, Do-Yun
Heo, Jung Ho
Kim, Chung Hui
Kim, Euikyung
Kim, Jong Shu
author_facet Kang, Changgeun
Lee, Hyungkyoung
Hah, Do-Yun
Heo, Jung Ho
Kim, Chung Hui
Kim, Euikyung
Kim, Jong Shu
author_sort Kang, Changgeun
collection PubMed
description Development of a therapy providing protection from, or reversing gentamicin-sulfate (GS)-induced oxidative stress and nephrotoxicity would be of great clinical significance. The present study was designed to investigate the protective effects of Houttuynia cordata Thunb. (HC) against gentamicin sulfate-induced renal damage in rats. Twenty-eight Sprague-Dawley rats were divided into 4 equal groups as follows: group 1, control; group 2, GS 100 mg/kg/d, intraperitoneal (i.p.) injection; group 3, GS 100 mg/kg/d, i.p. + HC 500 mg/kg/d, oral; and group 4, GS 100 mg/kg/d i.p. + HC 1000 mg/kg/d, oral administration). Treatments were administered once daily for 12 d. After 12 d, biochemical and histopathological analyses were conducted to evaluate oxidative stress and renal nephrotoxicity. Serum levels of creatinine, malondialdehyde (MDA), and blood urea nitrogen (BUN), together with renal levels of MDA, glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were quantified to evaluate antioxidant activity. Animals treated with GS alone showed a significant increase in serum levels of creatinine, BUN, and MDA, with decreased renal levels of GSH, SOD, and CAT. Treatment of rats with HC showed significant improvement in renal function, presumably as a result of decreased biochemical indices and oxidative stress parameters associated with GS-induced nephrotoxicity. Histopathological examination of the rat kidneys confirmed these observations. Therefore, the novel natural antioxidant HC may protect against GSinduced nephrotoxicity and oxidative stress in rats.
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spelling pubmed-38344372013-11-25 Protective Effects of Houttuynia cordata Thunb. on Gentamicin-induced Oxidative Stress and Nephrotoxicity in Rats Kang, Changgeun Lee, Hyungkyoung Hah, Do-Yun Heo, Jung Ho Kim, Chung Hui Kim, Euikyung Kim, Jong Shu Toxicol Res Articles Development of a therapy providing protection from, or reversing gentamicin-sulfate (GS)-induced oxidative stress and nephrotoxicity would be of great clinical significance. The present study was designed to investigate the protective effects of Houttuynia cordata Thunb. (HC) against gentamicin sulfate-induced renal damage in rats. Twenty-eight Sprague-Dawley rats were divided into 4 equal groups as follows: group 1, control; group 2, GS 100 mg/kg/d, intraperitoneal (i.p.) injection; group 3, GS 100 mg/kg/d, i.p. + HC 500 mg/kg/d, oral; and group 4, GS 100 mg/kg/d i.p. + HC 1000 mg/kg/d, oral administration). Treatments were administered once daily for 12 d. After 12 d, biochemical and histopathological analyses were conducted to evaluate oxidative stress and renal nephrotoxicity. Serum levels of creatinine, malondialdehyde (MDA), and blood urea nitrogen (BUN), together with renal levels of MDA, glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) were quantified to evaluate antioxidant activity. Animals treated with GS alone showed a significant increase in serum levels of creatinine, BUN, and MDA, with decreased renal levels of GSH, SOD, and CAT. Treatment of rats with HC showed significant improvement in renal function, presumably as a result of decreased biochemical indices and oxidative stress parameters associated with GS-induced nephrotoxicity. Histopathological examination of the rat kidneys confirmed these observations. Therefore, the novel natural antioxidant HC may protect against GSinduced nephrotoxicity and oxidative stress in rats. The Korean Society of Toxicology 2013-03 /pmc/articles/PMC3834437/ /pubmed/24278630 http://dx.doi.org/10.5487/TR.2013.29.1.061 Text en Copyright ©2013, The Korean Society of Toxicology http://creativecommons.org/licenses/by-nc/3.0/ This is an Open-Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Articles
Kang, Changgeun
Lee, Hyungkyoung
Hah, Do-Yun
Heo, Jung Ho
Kim, Chung Hui
Kim, Euikyung
Kim, Jong Shu
Protective Effects of Houttuynia cordata Thunb. on Gentamicin-induced Oxidative Stress and Nephrotoxicity in Rats
title Protective Effects of Houttuynia cordata Thunb. on Gentamicin-induced Oxidative Stress and Nephrotoxicity in Rats
title_full Protective Effects of Houttuynia cordata Thunb. on Gentamicin-induced Oxidative Stress and Nephrotoxicity in Rats
title_fullStr Protective Effects of Houttuynia cordata Thunb. on Gentamicin-induced Oxidative Stress and Nephrotoxicity in Rats
title_full_unstemmed Protective Effects of Houttuynia cordata Thunb. on Gentamicin-induced Oxidative Stress and Nephrotoxicity in Rats
title_short Protective Effects of Houttuynia cordata Thunb. on Gentamicin-induced Oxidative Stress and Nephrotoxicity in Rats
title_sort protective effects of houttuynia cordata thunb. on gentamicin-induced oxidative stress and nephrotoxicity in rats
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3834437/
https://www.ncbi.nlm.nih.gov/pubmed/24278630
http://dx.doi.org/10.5487/TR.2013.29.1.061
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