ISSN: 1449-1907International Journal of Medical Sciences
Global reach, higher impact
Int J Med Sci 2022; 19(4):740-752. doi:10.7150/ijms.69807 This issue Cite
Research Paper
N-acetylcysteine Ameliorates Vancomycin-induced Nephrotoxicity by Inhibiting Oxidative Stress and Apoptosis in the in vivo and in vitro Models
1. Department of Pharmacy, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
2. Department of General Surgery, Huadong Hospital, Fudan University, Shanghai, China.
3. Department of Pharmacology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
# Ping Yu and Jing Luo contributed equally to the study.
Citation:
Yu P, Luo J, Song H, Qian T, He X, Fang J, Dong W, Bian X. N-acetylcysteine Ameliorates Vancomycin-induced Nephrotoxicity by Inhibiting Oxidative Stress and Apoptosis in the in vivo and in vitro Models. Int J Med Sci 2022; 19(4):740-752. doi:10.7150/ijms.69807. https://www.medsci.org/v19p0740.htm
Other stylesAbstract
Background: Oxidative stress-related apoptosis is considered as the key mechanism implicated in the pathophysiology of nephrotoxicity with vancomycin (VCM) therapy. We evaluated the possible effects of N-acetylcysteine (NAC) on VCM-induced nephrotoxicity and the underlying mechanism.
Methods: VCM-induced nephrotoxicity was established using HK-2 cells and SD rats and observed by measuring cell survival, kidney histological changes, renal function and kidney injury related markers (KIM-1 and NGAL). Oxidative stress, renal cell apoptosis and the involved signaling pathways were also evaluated.
Results: In model rats, NAC could protect against VCM-induced acute kidney injury with histological damage, renal dysfunction, and increased Cre and BUN levels. In HK-2 cells, VCM-induced decreased cell viability was restored by NAC. In addition, increased expression of caspase-3, KIM-1 and NGAL suffering from VCM was also reversed by NAC in vivo and in vitro. NAC inhibited ROS production, decreased cell apoptosis by decreasing the Bax/Bcl-2 ratio and caspase-3 expression in HK-2 cells and regulated oxidative stress indicators in the kidney by decreasing GSH, SOD and CAT activity and increasing MDA levels. Furthermore, NAC could effectively reverse VCM-associated increased P38 MAPK/JNK phosphorylation.
Conclusions: The results demonstrated that NAC had a protective effect against nephrotoxicity from VCM by inhibiting oxidative stress and apoptosis via P38 MAPK/JNK.
Keywords: vancomycin, nephrotoxicity, N-acetylcysteine, oxidative stress, renal protection
Citation styles
APA
Yu, P., Luo, J., Song, H., Qian, T., He, X., Fang, J., Dong, W., Bian, X. (2022). N-acetylcysteine Ameliorates Vancomycin-induced Nephrotoxicity by Inhibiting Oxidative Stress and Apoptosis in the in vivo and in vitro Models. International Journal of Medical Sciences, 19(4), 740-752. https://doi.org/10.7150/ijms.69807.
ACS
Yu, P.; Luo, J.; Song, H.; Qian, T.; He, X.; Fang, J.; Dong, W.; Bian, X. N-acetylcysteine Ameliorates Vancomycin-induced Nephrotoxicity by Inhibiting Oxidative Stress and Apoptosis in the in vivo and in vitro Models. Int. J. Med. Sci. 2022, 19 (4), 740-752. DOI: 10.7150/ijms.69807.
NLM
Yu P, Luo J, Song H, Qian T, He X, Fang J, Dong W, Bian X. N-acetylcysteine Ameliorates Vancomycin-induced Nephrotoxicity by Inhibiting Oxidative Stress and Apoptosis in the in vivo and in vitro Models. Int J Med Sci 2022; 19(4):740-752. doi:10.7150/ijms.69807. https://www.medsci.org/v19p0740.htm
CSE
Yu P, Luo J, Song H, Qian T, He X, Fang J, Dong W, Bian X. 2022. N-acetylcysteine Ameliorates Vancomycin-induced Nephrotoxicity by Inhibiting Oxidative Stress and Apoptosis in the in vivo and in vitro Models. Int J Med Sci. 19(4):740-752.
This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.