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Protective effect of thymol on glycerol-induced acute kidney injury
Acute kidney injury (AKI) is a syndrome characterized by an accelerating decrease in renal function in a short time. Thymol is one of the main components of thyme species and has a variety of pharmacological effects. Here, we investigated whether thymol could ameliorate rhabdomyolysis (RM)-induced A...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Taylor & Francis
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10332232/ https://www.ncbi.nlm.nih.gov/pubmed/37417222 http://dx.doi.org/10.1080/0886022X.2023.2227728 |
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author | Wang, Qinglian Qi, Guanghui Zhou, Hongwei Cheng, Fajuan Yang, Xiaowei Liu, Xiang Wang, Rong |
author_facet | Wang, Qinglian Qi, Guanghui Zhou, Hongwei Cheng, Fajuan Yang, Xiaowei Liu, Xiang Wang, Rong |
author_sort | Wang, Qinglian |
collection | PubMed |
description | Acute kidney injury (AKI) is a syndrome characterized by an accelerating decrease in renal function in a short time. Thymol is one of the main components of thyme species and has a variety of pharmacological effects. Here, we investigated whether thymol could ameliorate rhabdomyolysis (RM)-induced AKI and its related mechanism. Glycerol was used to induce RM-associated AKI in rats. Rats received thymol (20 mg/kg/day or 40 mg/kg/day) gavage 24 h before glycerol injection until 72 h after injection daily. Kidney injury was identified by measuring serum creatinine (Scr) and urea levels and by H&E and PAS staining and immunohistochemistry (the expression of proliferating cell nuclear antigen (PCNA)). Renal superoxide dismutase (SOD), malondialdehyde (MDA), and oxidative stress-related Nrf2/HO-1 signaling pathways were measured. The expression of the inflammatory markers TNF-α, IL-6, MCP-1, and NF-κB was assessed by ELISA and western blotting. Finally, the expression of the PI3K/Akt signaling pathway was detected by western blotting. Glycerol administration induced obvious renal histologic damage and increased Scr, urea, and PCNA expression. Notably, thymol treatment attenuated these structural and functional changes and prevented renal oxidative stress, inflammatory damage and PI3K/Akt pathway downregulation associated with glycerol-induced AKI. In conclusion, thymol might have potential applications in the amelioration of AKI via its antioxidant and anti-inflammatory effects and upregulation of the PI3K/Akt signaling pathway. |
format | Online Article Text |
id | pubmed-10332232 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Taylor & Francis |
record_format | MEDLINE/PubMed |
spelling | pubmed-103322322023-07-11 Protective effect of thymol on glycerol-induced acute kidney injury Wang, Qinglian Qi, Guanghui Zhou, Hongwei Cheng, Fajuan Yang, Xiaowei Liu, Xiang Wang, Rong Ren Fail Laboratory Study Acute kidney injury (AKI) is a syndrome characterized by an accelerating decrease in renal function in a short time. Thymol is one of the main components of thyme species and has a variety of pharmacological effects. Here, we investigated whether thymol could ameliorate rhabdomyolysis (RM)-induced AKI and its related mechanism. Glycerol was used to induce RM-associated AKI in rats. Rats received thymol (20 mg/kg/day or 40 mg/kg/day) gavage 24 h before glycerol injection until 72 h after injection daily. Kidney injury was identified by measuring serum creatinine (Scr) and urea levels and by H&E and PAS staining and immunohistochemistry (the expression of proliferating cell nuclear antigen (PCNA)). Renal superoxide dismutase (SOD), malondialdehyde (MDA), and oxidative stress-related Nrf2/HO-1 signaling pathways were measured. The expression of the inflammatory markers TNF-α, IL-6, MCP-1, and NF-κB was assessed by ELISA and western blotting. Finally, the expression of the PI3K/Akt signaling pathway was detected by western blotting. Glycerol administration induced obvious renal histologic damage and increased Scr, urea, and PCNA expression. Notably, thymol treatment attenuated these structural and functional changes and prevented renal oxidative stress, inflammatory damage and PI3K/Akt pathway downregulation associated with glycerol-induced AKI. In conclusion, thymol might have potential applications in the amelioration of AKI via its antioxidant and anti-inflammatory effects and upregulation of the PI3K/Akt signaling pathway. Taylor & Francis 2023-07-07 /pmc/articles/PMC10332232/ /pubmed/37417222 http://dx.doi.org/10.1080/0886022X.2023.2227728 Text en © 2023 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent. |
spellingShingle | Laboratory Study Wang, Qinglian Qi, Guanghui Zhou, Hongwei Cheng, Fajuan Yang, Xiaowei Liu, Xiang Wang, Rong Protective effect of thymol on glycerol-induced acute kidney injury |
title | Protective effect of thymol on glycerol-induced acute kidney injury |
title_full | Protective effect of thymol on glycerol-induced acute kidney injury |
title_fullStr | Protective effect of thymol on glycerol-induced acute kidney injury |
title_full_unstemmed | Protective effect of thymol on glycerol-induced acute kidney injury |
title_short | Protective effect of thymol on glycerol-induced acute kidney injury |
title_sort | protective effect of thymol on glycerol-induced acute kidney injury |
topic | Laboratory Study |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10332232/ https://www.ncbi.nlm.nih.gov/pubmed/37417222 http://dx.doi.org/10.1080/0886022X.2023.2227728 |
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