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Effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats

Aim of the present study was to assess the hepatoprotective activity of goat milk on antitubercular drug-induced hepatotoxicity in rats. Hepatotoxicity was induced in rats using a combination of isoniazid, rifampicin, and pyrazinamide given orally as a suspension for 30 days. Treatment groups receiv...

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Autores principales: Miglani, Sonam, Patyar, Rakesh Raman, Patyar, Sazal, Reshi, Mohammad Rafi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taiwan Food and Drug Administration 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9337283/
https://www.ncbi.nlm.nih.gov/pubmed/28911608
http://dx.doi.org/10.1016/j.jfda.2016.03.012
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author Miglani, Sonam
Patyar, Rakesh Raman
Patyar, Sazal
Reshi, Mohammad Rafi
author_facet Miglani, Sonam
Patyar, Rakesh Raman
Patyar, Sazal
Reshi, Mohammad Rafi
author_sort Miglani, Sonam
collection PubMed
description Aim of the present study was to assess the hepatoprotective activity of goat milk on antitubercular drug-induced hepatotoxicity in rats. Hepatotoxicity was induced in rats using a combination of isoniazid, rifampicin, and pyrazinamide given orally as a suspension for 30 days. Treatment groups received goat milk along with antitubercular drugs. Liver damage was assessed using biochemical and histological parameters. Administration of goat milk (20 mL/kg) along with antitubercular drugs (Group III) reversed the levels of serum alanine aminotransferase (82 ± 25.1 vs. 128.8 ± 8.9 units/L) and aspartate aminotransferase (174.7 ± 31.5 vs. 296.4 ± 56.4 units/L, p < 0.01) compared with antitubercular drug treatment Group II. There was a significant decrease in serum alanine aminotransferase (41.8 ± 4.1 vs. 128.8 ± 8.9 units/L, p < 0.01) and aspartate aminotransferase (128.8 ± 8.54 vs. 296.4 ± 56.4 units/L, p < 0.001) levels in Group IV (goat milk 40 mL/kg) compared with antitubercular drug treatment Group II. Goat milk (20 mL/kg and 40 mL/kg) was effective in reversing the rise in malondialdehyde level compared with the antitubercular drug suspension groups (58.5 ± 2 vs. 89.88 ± 2.42 μmol/mL of tissue homogenate, p < 0.001 and 69.7 ± 0.78 vs. 89.88 ± 2.42 μmol/mL of tissue homogenate, p < 0.001, respectively). Similarly, both doses of milk significantly prevented a fall in superoxide dismutase level (6.23 ± 0.29 vs. 3.1 ± 0.288 units/mL, p < 0.001 and 7.8 ± 0.392 vs. 3.1 ± 0.288 units/mL, p < 0.001) compared with the group receiving antitubercular drugs alone. Histological examination indicated that goat milk reduced inflammation and necrotic changes in hepatocytes in the treatment groups. The results indicated that goat milk prevented the antitubercular drug-induced hepatotoxicity and is an effective hepatoprotective agent.
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spelling pubmed-93372832022-08-09 Effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats Miglani, Sonam Patyar, Rakesh Raman Patyar, Sazal Reshi, Mohammad Rafi J Food Drug Anal Original Article Aim of the present study was to assess the hepatoprotective activity of goat milk on antitubercular drug-induced hepatotoxicity in rats. Hepatotoxicity was induced in rats using a combination of isoniazid, rifampicin, and pyrazinamide given orally as a suspension for 30 days. Treatment groups received goat milk along with antitubercular drugs. Liver damage was assessed using biochemical and histological parameters. Administration of goat milk (20 mL/kg) along with antitubercular drugs (Group III) reversed the levels of serum alanine aminotransferase (82 ± 25.1 vs. 128.8 ± 8.9 units/L) and aspartate aminotransferase (174.7 ± 31.5 vs. 296.4 ± 56.4 units/L, p < 0.01) compared with antitubercular drug treatment Group II. There was a significant decrease in serum alanine aminotransferase (41.8 ± 4.1 vs. 128.8 ± 8.9 units/L, p < 0.01) and aspartate aminotransferase (128.8 ± 8.54 vs. 296.4 ± 56.4 units/L, p < 0.001) levels in Group IV (goat milk 40 mL/kg) compared with antitubercular drug treatment Group II. Goat milk (20 mL/kg and 40 mL/kg) was effective in reversing the rise in malondialdehyde level compared with the antitubercular drug suspension groups (58.5 ± 2 vs. 89.88 ± 2.42 μmol/mL of tissue homogenate, p < 0.001 and 69.7 ± 0.78 vs. 89.88 ± 2.42 μmol/mL of tissue homogenate, p < 0.001, respectively). Similarly, both doses of milk significantly prevented a fall in superoxide dismutase level (6.23 ± 0.29 vs. 3.1 ± 0.288 units/mL, p < 0.001 and 7.8 ± 0.392 vs. 3.1 ± 0.288 units/mL, p < 0.001) compared with the group receiving antitubercular drugs alone. Histological examination indicated that goat milk reduced inflammation and necrotic changes in hepatocytes in the treatment groups. The results indicated that goat milk prevented the antitubercular drug-induced hepatotoxicity and is an effective hepatoprotective agent. Taiwan Food and Drug Administration 2016-06-02 /pmc/articles/PMC9337283/ /pubmed/28911608 http://dx.doi.org/10.1016/j.jfda.2016.03.012 Text en © 2016 Taiwan Food and Drug Administration https://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/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) ).
spellingShingle Original Article
Miglani, Sonam
Patyar, Rakesh Raman
Patyar, Sazal
Reshi, Mohammad Rafi
Effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats
title Effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats
title_full Effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats
title_fullStr Effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats
title_full_unstemmed Effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats
title_short Effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats
title_sort effect of goat milk on hepatotoxicity induced by antitubercular drugs in rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9337283/
https://www.ncbi.nlm.nih.gov/pubmed/28911608
http://dx.doi.org/10.1016/j.jfda.2016.03.012
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