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Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver

BACKGROUND: Carbon tetra chloride (CCl(4)), an industrial solvent, is a hepatotoxic agent and it is the well established animal model for free radical-induced liver injury. The present investigation was carried out to establish the protective effect of natansnin, a novel dibenzoyl glycoside from Sal...

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Autores principales: Srilaxmi, Polimetla, Sareddy, Gangadhara Reddy, kishor, Polavarapu Bilhan Kavi, Setty, Oruganti Hussainaiah, Babu, Phanithi Prakash
Formato: Texto
Lenguaje:English
Publicado: BioMed Central 2010
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967507/
https://www.ncbi.nlm.nih.gov/pubmed/20939865
http://dx.doi.org/10.1186/1471-2210-10-13
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author Srilaxmi, Polimetla
Sareddy, Gangadhara Reddy
kishor, Polavarapu Bilhan Kavi
Setty, Oruganti Hussainaiah
Babu, Phanithi Prakash
author_facet Srilaxmi, Polimetla
Sareddy, Gangadhara Reddy
kishor, Polavarapu Bilhan Kavi
Setty, Oruganti Hussainaiah
Babu, Phanithi Prakash
author_sort Srilaxmi, Polimetla
collection PubMed
description BACKGROUND: Carbon tetra chloride (CCl(4)), an industrial solvent, is a hepatotoxic agent and it is the well established animal model for free radical-induced liver injury. The present investigation was carried out to establish the protective effect of natansnin, a novel dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver. RESULTS: CCl(4 )significantly increased the levels of lipid peroxides, oxidized glutathione and decreased the levels of reduced glutathione, SOD and CAT. CCl(4 )induce marked histopathological changes and increase in the levels of apoptotic proteins. CCl(4 )treatment significantly increased the levels of apoptotic proteins such as caspases-3, PARP, Bax, Bid and cytochrome C and also increased the levels of inflammatory mediators iNos and Cox-2. Natansnin treatment significantly decreased the levels of CCl(4 )induced apoptotic proteins and inflammatory mediators. Further natansinin treatment significantly inhibited the CCl(4 )induced apoptosis which was evident form the reduced TUNEL positive cells. CONCLUSIONS: In conclusion, our study demonstrated the protective effect of natansnin against CCl(4 )induced oxidative stress and cellular degeneration in rat liver tissue. This protective effect of natansnin can be correlated to its direct antioxidant effect.
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spelling pubmed-29675072010-11-03 Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver Srilaxmi, Polimetla Sareddy, Gangadhara Reddy kishor, Polavarapu Bilhan Kavi Setty, Oruganti Hussainaiah Babu, Phanithi Prakash BMC Pharmacol Research Article BACKGROUND: Carbon tetra chloride (CCl(4)), an industrial solvent, is a hepatotoxic agent and it is the well established animal model for free radical-induced liver injury. The present investigation was carried out to establish the protective effect of natansnin, a novel dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver. RESULTS: CCl(4 )significantly increased the levels of lipid peroxides, oxidized glutathione and decreased the levels of reduced glutathione, SOD and CAT. CCl(4 )induce marked histopathological changes and increase in the levels of apoptotic proteins. CCl(4 )treatment significantly increased the levels of apoptotic proteins such as caspases-3, PARP, Bax, Bid and cytochrome C and also increased the levels of inflammatory mediators iNos and Cox-2. Natansnin treatment significantly decreased the levels of CCl(4 )induced apoptotic proteins and inflammatory mediators. Further natansinin treatment significantly inhibited the CCl(4 )induced apoptosis which was evident form the reduced TUNEL positive cells. CONCLUSIONS: In conclusion, our study demonstrated the protective effect of natansnin against CCl(4 )induced oxidative stress and cellular degeneration in rat liver tissue. This protective effect of natansnin can be correlated to its direct antioxidant effect. BioMed Central 2010-10-12 /pmc/articles/PMC2967507/ /pubmed/20939865 http://dx.doi.org/10.1186/1471-2210-10-13 Text en Copyright ©2010 Srilaxmi et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Srilaxmi, Polimetla
Sareddy, Gangadhara Reddy
kishor, Polavarapu Bilhan Kavi
Setty, Oruganti Hussainaiah
Babu, Phanithi Prakash
Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver
title Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver
title_full Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver
title_fullStr Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver
title_full_unstemmed Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver
title_short Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl(4 )induced oxidative stress and cellular degeneration in rat liver
title_sort protective efficacy of natansnin, a dibenzoyl glycoside from salvinia natans against ccl(4 )induced oxidative stress and cellular degeneration in rat liver
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2967507/
https://www.ncbi.nlm.nih.gov/pubmed/20939865
http://dx.doi.org/10.1186/1471-2210-10-13
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