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Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats

BACKGROUND: Cadmium (Cd), a nonessential heavy metal, is a major environmental and public health concern. Oxidative stress plays an important role in Cd-induced kidney dysfunction. Tinospora cordifolia, a medicinal plant rich in phytochemicals, possesses antioxidant activity. The objective of the pr...

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Autores principales: Padma, Viswanadha Vijaya, Baskaran, Rathinasamy, Divya, Subramani, Priya, Lohanathan Bharathi, Saranya, Sithuraj
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381431/
https://www.ncbi.nlm.nih.gov/pubmed/28462097
http://dx.doi.org/10.1016/j.imr.2015.12.005
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author Padma, Viswanadha Vijaya
Baskaran, Rathinasamy
Divya, Subramani
Priya, Lohanathan Bharathi
Saranya, Sithuraj
author_facet Padma, Viswanadha Vijaya
Baskaran, Rathinasamy
Divya, Subramani
Priya, Lohanathan Bharathi
Saranya, Sithuraj
author_sort Padma, Viswanadha Vijaya
collection PubMed
description BACKGROUND: Cadmium (Cd), a nonessential heavy metal, is a major environmental and public health concern. Oxidative stress plays an important role in Cd-induced kidney dysfunction. Tinospora cordifolia, a medicinal plant rich in phytochemicals, possesses antioxidant activity. The objective of the present study was to assess the protective effect of Tinospora cordifolia-stem methanolic extract (TCE) on Cd-induced nephrotoxicity in Wistar rats. METHODS: Male Wistar rats were administered ∼5 mg/kg body weight Cd orally and 100 mg/kg body weight TCE for 28 days. At the end of Cd and TCE treatment, biochemical assays were performed in serum and tissue homogenate. RESULTS: Cd-induced oxidative stress in the kidney resulted in increased levels of lipid peroxidation and protein carbonyl content with a significant decrease in cellular antioxidants, such as reduced GSH, SOD, CAT, GPX, and GST. Cd-induced nephrotoxicity was further confirmed by marked changes in the histology of the kidney and increased levels of kidney markers. Additionally, Cd-treated rats showed alterations in membrane-bound ATPase activity and decreased levels of tissue glycoproteins. Cotreatment with TCE considerably reduced the biochemical alterations in serum and renal tissue induced by Cd, and also restored ATPase activity and glycoproteins to near normal levels. CONCLUSION: Our results suggested that TCE with its antioxidant effect offered cytoprotection against Cd-induced toxicity in kidneys by restoring the altered cellular antioxidants and renal markers. TCE treatment for 28 days reversed ATPase activity and tissue glycoprotein levels. These results revealed the protective effect of TCE on Cd-induced toxicity in kidneys and oxidative stress.
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spelling pubmed-53814312017-05-01 Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats Padma, Viswanadha Vijaya Baskaran, Rathinasamy Divya, Subramani Priya, Lohanathan Bharathi Saranya, Sithuraj Integr Med Res Original Article BACKGROUND: Cadmium (Cd), a nonessential heavy metal, is a major environmental and public health concern. Oxidative stress plays an important role in Cd-induced kidney dysfunction. Tinospora cordifolia, a medicinal plant rich in phytochemicals, possesses antioxidant activity. The objective of the present study was to assess the protective effect of Tinospora cordifolia-stem methanolic extract (TCE) on Cd-induced nephrotoxicity in Wistar rats. METHODS: Male Wistar rats were administered ∼5 mg/kg body weight Cd orally and 100 mg/kg body weight TCE for 28 days. At the end of Cd and TCE treatment, biochemical assays were performed in serum and tissue homogenate. RESULTS: Cd-induced oxidative stress in the kidney resulted in increased levels of lipid peroxidation and protein carbonyl content with a significant decrease in cellular antioxidants, such as reduced GSH, SOD, CAT, GPX, and GST. Cd-induced nephrotoxicity was further confirmed by marked changes in the histology of the kidney and increased levels of kidney markers. Additionally, Cd-treated rats showed alterations in membrane-bound ATPase activity and decreased levels of tissue glycoproteins. Cotreatment with TCE considerably reduced the biochemical alterations in serum and renal tissue induced by Cd, and also restored ATPase activity and glycoproteins to near normal levels. CONCLUSION: Our results suggested that TCE with its antioxidant effect offered cytoprotection against Cd-induced toxicity in kidneys by restoring the altered cellular antioxidants and renal markers. TCE treatment for 28 days reversed ATPase activity and tissue glycoprotein levels. These results revealed the protective effect of TCE on Cd-induced toxicity in kidneys and oxidative stress. Elsevier 2016-03 2016-01-08 /pmc/articles/PMC5381431/ /pubmed/28462097 http://dx.doi.org/10.1016/j.imr.2015.12.005 Text en © 2016 Korea Institute of Oriental Medicine. Published by Elsevier. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Original Article
Padma, Viswanadha Vijaya
Baskaran, Rathinasamy
Divya, Subramani
Priya, Lohanathan Bharathi
Saranya, Sithuraj
Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats
title Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats
title_full Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats
title_fullStr Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats
title_full_unstemmed Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats
title_short Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats
title_sort modulatory effect of tinospora cordifolia extract on cd-induced oxidative stress in wistar rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381431/
https://www.ncbi.nlm.nih.gov/pubmed/28462097
http://dx.doi.org/10.1016/j.imr.2015.12.005
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