Protective Effect of Silymarin and Gallic Acid against Cisplatin-Induced Nephrotoxicity and Hepatotoxicity
Objective. This study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. Materials and Methods. In the study, 56 Wistar Albino rats were equally divided into eight groups. Group 1 was the control group; group 2 was the group r...
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Published in | International journal of clinical practice (Esher) Vol. 2022; pp. 6541026 - 10 |
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Format | Journal Article |
Language | English |
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2022
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Abstract | Objective. This study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. Materials and Methods. In the study, 56 Wistar Albino rats were equally divided into eight groups. Group 1 was the control group; group 2 was the group receiving cisplatin; group 3 was the group receiving cisplatin + gallic acid; group 4 was the group receiving cisplatin + silymarin; group 5 was the group receiving cisplatin + silymarin + gallic acid; group 6 was the group receiving silymarin; group 7 was the group receiving gallic acid; group 8 was the group receiving gallic acid + silymarin. AST, ALT, urea, creatinine, albumin, globulin, and total protein levels were measured at the end of the study. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione (GSH), and 8-hydroxy-2′-deoxyguanosine (8OH-dG) levels were measured in kidney and liver tissues. Additionally, histopathological evaluations of the tissues were also performed. Results. In kidney and liver tissues, cisplatin significantly increased MDA and 8-OHdG levels compared with treatment groups (p<0.05). Silymarin-treated group significantly increased the SOD activity and GSH amount in the liver tissue compared with the cisplatin-treated group (p<0.05). Gallic acid significantly increased CAT activity compared with the cisplatin-treated group (p<0.05). It was determined that the cisplatin-treated group significantly decreased CAT and SOD activity compared with the control group (p>0.05). Gallic acid showed a significant increase in CAT and SOD activity in kidney tissue compared with the cisplatin-treated group (p<0.05). Conclusion. As a result, it was observed that gallic acid silymarin had a protective effect on cisplatin-induced nephrotoxic and hepatotoxic effects. |
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AbstractList | Objective. This study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. Materials and Methods. In the study, 56 Wistar Albino rats were equally divided into eight groups. Group 1 was the control group; group 2 was the group receiving cisplatin; group 3 was the group receiving cisplatin + gallic acid; group 4 was the group receiving cisplatin + silymarin; group 5 was the group receiving cisplatin + silymarin + gallic acid; group 6 was the group receiving silymarin; group 7 was the group receiving gallic acid; group 8 was the group receiving gallic acid + silymarin. AST, ALT, urea, creatinine, albumin, globulin, and total protein levels were measured at the end of the study. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione (GSH), and 8-hydroxy-2′-deoxyguanosine (8OH-dG) levels were measured in kidney and liver tissues. Additionally, histopathological evaluations of the tissues were also performed. Results. In kidney and liver tissues, cisplatin significantly increased MDA and 8-OHdG levels compared with treatment groups (p<0.05). Silymarin-treated group significantly increased the SOD activity and GSH amount in the liver tissue compared with the cisplatin-treated group (p<0.05). Gallic acid significantly increased CAT activity compared with the cisplatin-treated group (p<0.05). It was determined that the cisplatin-treated group significantly decreased CAT and SOD activity compared with the control group (p>0.05). Gallic acid showed a significant increase in CAT and SOD activity in kidney tissue compared with the cisplatin-treated group (p<0.05). Conclusion. As a result, it was observed that gallic acid silymarin had a protective effect on cisplatin-induced nephrotoxic and hepatotoxic effects. ObjectiveThis study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. Materials and MethodsIn the study, 56 Wistar Albino rats were equally divided into eight groups. Group 1 was the control group; group 2 was the group receiving cisplatin; group 3 was the group receiving cisplatin + gallic acid; group 4 was the group receiving cisplatin + silymarin; group 5 was the group receiving cisplatin + silymarin + gallic acid; group 6 was the group receiving silymarin; group 7 was the group receiving gallic acid; group 8 was the group receiving gallic acid + silymarin. AST, ALT, urea, creatinine, albumin, globulin, and total protein levels were measured at the end of the study. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione (GSH), and 8-hydroxy-2'-deoxyguanosine (8OH-dG) levels were measured in kidney and liver tissues. Additionally, histopathological evaluations of the tissues were also performed. ResultsIn kidney and liver tissues, cisplatin significantly increased MDA and 8-OHdG levels compared with treatment groups (p < 0.05). Silymarin-treated group significantly increased the SOD activity and GSH amount in the liver tissue compared with the cisplatin-treated group (p < 0.05). Gallic acid significantly increased CAT activity compared with the cisplatin-treated group (p < 0.05). It was determined that the cisplatin-treated group significantly decreased CAT and SOD activity compared with the control group (p > 0.05). Gallic acid showed a significant increase in CAT and SOD activity in kidney tissue compared with the cisplatin-treated group (p < 0.05). ConclusionAs a result, it was observed that gallic acid silymarin had a protective effect on cisplatin-induced nephrotoxic and hepatotoxic effects. This study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. In the study, 56 Wistar Albino rats were equally divided into eight groups. Group 1 was the control group; group 2 was the group receiving cisplatin; group 3 was the group receiving cisplatin + gallic acid; group 4 was the group receiving cisplatin + silymarin; group 5 was the group receiving cisplatin + silymarin + gallic acid; group 6 was the group receiving silymarin; group 7 was the group receiving gallic acid; group 8 was the group receiving gallic acid + silymarin. AST, ALT, urea, creatinine, albumin, globulin, and total protein levels were measured at the end of the study. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione (GSH), and 8-hydroxy-2'-deoxyguanosine (8OH-dG) levels were measured in kidney and liver tissues. Additionally, histopathological evaluations of the tissues were also performed. In kidney and liver tissues, cisplatin significantly increased MDA and 8-OHdG levels compared with treatment groups ( < 0.05). Silymarin-treated group significantly increased the SOD activity and GSH amount in the liver tissue compared with the cisplatin-treated group ( < 0.05). Gallic acid significantly increased CAT activity compared with the cisplatin-treated group ( < 0.05). It was determined that the cisplatin-treated group significantly decreased CAT and SOD activity compared with the control group ( > 0.05). Gallic acid showed a significant increase in CAT and SOD activity in kidney tissue compared with the cisplatin-treated group ( < 0.05). As a result, it was observed that gallic acid silymarin had a protective effect on cisplatin-induced nephrotoxic and hepatotoxic effects. Objective. This study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. Materials and Methods. In the study, 56 Wistar Albino rats were equally divided into eight groups. Group 1 was the control group; group 2 was the group receiving cisplatin; group 3 was the group receiving cisplatin + gallic acid; group 4 was the group receiving cisplatin + silymarin; group 5 was the group receiving cisplatin + silymarin + gallic acid; group 6 was the group receiving silymarin; group 7 was the group receiving gallic acid; group 8 was the group receiving gallic acid + silymarin. AST, ALT, urea, creatinine, albumin, globulin, and total protein levels were measured at the end of the study. Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), glutathione (GSH), and 8-hydroxy-2′-deoxyguanosine (8OH-dG) levels were measured in kidney and liver tissues. Additionally, histopathological evaluations of the tissues were also performed. Results. In kidney and liver tissues, cisplatin significantly increased MDA and 8-OHdG levels compared with treatment groups ( p < 0.05 ). Silymarin-treated group significantly increased the SOD activity and GSH amount in the liver tissue compared with the cisplatin-treated group ( p < 0.05 ). Gallic acid significantly increased CAT activity compared with the cisplatin-treated group ( p < 0.05 ). It was determined that the cisplatin-treated group significantly decreased CAT and SOD activity compared with the control group ( p > 0.05 ). Gallic acid showed a significant increase in CAT and SOD activity in kidney tissue compared with the cisplatin-treated group ( p < 0.05 ). Conclusion. As a result, it was observed that gallic acid silymarin had a protective effect on cisplatin-induced nephrotoxic and hepatotoxic effects. |
Author | Doğan, Duygu Kömüroğlu, Ahmet Ufuk Meydan, İsmet |
AuthorAffiliation | Van Yuzuncu Yil University, Vocational School of Health Services, Van, Turkey |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/35685593$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1016_j_bse_2024_104792 crossref_primary_10_1016_j_jsps_2023_101730 crossref_primary_10_1007_s11356_023_30197_1 crossref_primary_10_1177_1098612X231173519 crossref_primary_10_1016_j_foodres_2024_114068 crossref_primary_10_4274_haseki_galenos_2022_8098 crossref_primary_10_46876_ja_1298971 crossref_primary_10_1007_s00228_022_03434_8 |
Cites_doi | 10.1111/dth.13236 10.1111/jfbc.13190 10.1016/j.pharep.2017.03.011 10.1080/00015458.2017.1394672 10.1007/s00580-019-03055-1 10.1053/j.gastro.2009.09.021 10.1007/s10637-009-9241-9 10.1016/j.tox.2006.11.073 10.3390/toxins2112490 10.1111/jfbc.12398 10.1016/s0014-5793(97)00523-1 10.3390/medsci3030078 10.1016/j.fct.2010.05.004 10.1016/j.bbadis.2020.165911 10.1080/07391102.2017.1305297 10.1590/s0102-865020170080000005 10.1016/0002-9343(91)90279-7 10.1155/2018/1630751 10.3390/antiox4010204 10.1016/j.bjorl.2018.03.001 10.1111/liv.14030 10.1080/0886022x.2018.1456938 10.1016/j.ejphar.2014.07.025 10.1039/c8tx00058a |
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Copyright | Copyright © 2022 Duygu Doğan et al. Copyright © 2022 Duygu Doğan et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0 Copyright © 2022 Duygu Doğan et al. 2022 |
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Snippet | Objective. This study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. Materials... This study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. In the study, 56 Wistar... ObjectiveThis study aimed to investigate the effects of gallic acid and silymarin against nephrotoxicity and hepatotoxicity caused by cisplatin. Materials and... |
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SubjectTerms | Acids Animals Antioxidants Antioxidants - pharmacology Antioxidants - therapeutic use Chemical and Drug Induced Liver Injury - metabolism Chemical and Drug Induced Liver Injury - pathology Chemical and Drug Induced Liver Injury - prevention & control Cisplatin Cisplatin - metabolism Cisplatin - toxicity Creatinine Deoxyguanosine Enzymes Free radicals Gallic acid Gallic Acid - metabolism Gallic Acid - pharmacology Gallic Acid - therapeutic use Globulins Glutathione Glutathione - metabolism Glutathione - pharmacology Hepatotoxicity Humans Ketamine Kidney Kidneys Liver Oxidative Stress Rats Rats, Wistar Silymarin Silymarin - metabolism Silymarin - pharmacology Statistical analysis Superoxide dismutase Superoxide Dismutase - metabolism Superoxide Dismutase - pharmacology Toxicity |
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Title | Protective Effect of Silymarin and Gallic Acid against Cisplatin-Induced Nephrotoxicity and Hepatotoxicity |
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