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Allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats
BACKGROUND: The aim of the present study was to evaluate the neuroprotective effect of allantoin in cisplatin‐induced toxicity in rats. METHODS: Adult male Wistar rats weighing 160‐200 g were used. Neuropathy was induced by injecting cisplatin (2 mg/kg, ip, twice a week for 6 weeks) and the rats wer...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6601039/ https://www.ncbi.nlm.nih.gov/pubmed/31392304 http://dx.doi.org/10.1002/ame2.12070 |
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author | N S, Vindya Mohamad, Aqib Razdan, Rema |
author_facet | N S, Vindya Mohamad, Aqib Razdan, Rema |
author_sort | N S, Vindya |
collection | PubMed |
description | BACKGROUND: The aim of the present study was to evaluate the neuroprotective effect of allantoin in cisplatin‐induced toxicity in rats. METHODS: Adult male Wistar rats weighing 160‐200 g were used. Neuropathy was induced by injecting cisplatin (2 mg/kg, ip, twice a week for 6 weeks) and the rats were concurrently treated with allantoin (200 and 400 mg/kg, po) for 8 weeks. At the end of the study, body weight and hemogram were measured. Behavioural tests were performed, including tests for cold and hot hyperalgesia, motor co‐ordination, locomotor activity, mechano‐tactile allodynia and mechanical hyperalgesia. The rats were then sacrificed and sciatic nerve conduction velocity was determined. The antioxidant enzyme and nitric oxide levels in sciatic nerve homogenates were measured. RESULTS: In this study, allantoin restored the motor nerve conduction velocity deficits induced by cisplatin, and the allantoin‐treated rats showed improvement in cold and thermal hyperalgesia, mechano‐tactile allodynia, and mechanical hyperalgesia. Allantoin treatment also improved the rats’ hematological status, increasing haemoglobin, platelet and RBC counts compared to the cisplatin‐treated group. Allantoin treatment also mitigated the functional abnormalities seen in the cisplatin neuropathy group, protecting neurons from the neurotoxic effects of cisplatin. CONCLUSION: Allantoin shows promise for use as an adjuvant drug in cancer treatment to protect against cisplatin‐induced neuropathy. |
format | Online Article Text |
id | pubmed-6601039 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-66010392019-08-07 Allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats N S, Vindya Mohamad, Aqib Razdan, Rema Animal Model Exp Med Original Articles BACKGROUND: The aim of the present study was to evaluate the neuroprotective effect of allantoin in cisplatin‐induced toxicity in rats. METHODS: Adult male Wistar rats weighing 160‐200 g were used. Neuropathy was induced by injecting cisplatin (2 mg/kg, ip, twice a week for 6 weeks) and the rats were concurrently treated with allantoin (200 and 400 mg/kg, po) for 8 weeks. At the end of the study, body weight and hemogram were measured. Behavioural tests were performed, including tests for cold and hot hyperalgesia, motor co‐ordination, locomotor activity, mechano‐tactile allodynia and mechanical hyperalgesia. The rats were then sacrificed and sciatic nerve conduction velocity was determined. The antioxidant enzyme and nitric oxide levels in sciatic nerve homogenates were measured. RESULTS: In this study, allantoin restored the motor nerve conduction velocity deficits induced by cisplatin, and the allantoin‐treated rats showed improvement in cold and thermal hyperalgesia, mechano‐tactile allodynia, and mechanical hyperalgesia. Allantoin treatment also improved the rats’ hematological status, increasing haemoglobin, platelet and RBC counts compared to the cisplatin‐treated group. Allantoin treatment also mitigated the functional abnormalities seen in the cisplatin neuropathy group, protecting neurons from the neurotoxic effects of cisplatin. CONCLUSION: Allantoin shows promise for use as an adjuvant drug in cancer treatment to protect against cisplatin‐induced neuropathy. John Wiley and Sons Inc. 2019-07-01 /pmc/articles/PMC6601039/ /pubmed/31392304 http://dx.doi.org/10.1002/ame2.12070 Text en © 2019 The Authors. Animal Models and Experimental Medicine published by John Wiley & Sons Australia, Ltd on behalf of The Chinese Association for Laboratory Animal Sciences This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Original Articles N S, Vindya Mohamad, Aqib Razdan, Rema Allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats |
title | Allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats |
title_full | Allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats |
title_fullStr | Allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats |
title_full_unstemmed | Allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats |
title_short | Allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats |
title_sort | allantoin attenuates deficits of behavioural and motor nerve conduction in an animal model of cisplatin‐induced neurotoxicity in rats |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6601039/ https://www.ncbi.nlm.nih.gov/pubmed/31392304 http://dx.doi.org/10.1002/ame2.12070 |
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