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N-Acetylcysteine Attenuates Cisplatin-Induced Acute Kidney Injury by Inhibiting the C5a Receptor
- Source :
- BioMed Research International, Vol 2019 (2019), BioMed Research International
- Publication Year :
- 2019
- Publisher :
- Hindawi Limited, 2019.
-
Abstract
- N-acetylcysteine has been widely used as a nutritional supplement and drug in humans for its antioxidant properties. The complement activation fragment C5a is a strong proinflammatory molecule that mediates cell adhesion, chemotaxis, and the complex biological functions. However, the effect of NAC on the C5a, and the relationship of those two with cisplatin-induced acute kidney injury are unknown. In cisplatin induced AKI mouse model, mice with NAC administration had a marked improvement in renal function (BUN and Cr), decreased pathological damage, reduced inflammation, and alleviated renal oxidative stress. Furthermore, C5a and C5aR expression in the cisplatin-treated group was notably increased compared with the control group, and this increase could be significantly inhibited by NAC. In addition, neutrophils coexpressed distinctly with C5aR, and the number of infiltrating neutrophils (MPO+ly6G+) and inflammatory factors decreased with NAC treatment in the cisplatin-treated group. Overall, these data demonstrate that NAC could ameliorate cisplatin-induced nephrotoxicity in mice and the protective effects may be conducted by inhibiting the activation of kidney inflammation and the complement system.
- Subjects :
- 0301 basic medicine
Article Subject
lcsh:Medicine
Inflammation
Pharmacology
medicine.disease_cause
General Biochemistry, Genetics and Molecular Biology
C5a receptor
Proinflammatory cytokine
Nephrotoxicity
Acetylcysteine
03 medical and health sciences
0302 clinical medicine
medicine
Receptor
General Immunology and Microbiology
Chemistry
lcsh:R
Acute kidney injury
General Medicine
medicine.disease
030104 developmental biology
030220 oncology & carcinogenesis
medicine.symptom
Oxidative stress
Research Article
medicine.drug
Subjects
Details
- ISSN :
- 23146141 and 23146133
- Volume :
- 2019
- Database :
- OpenAIRE
- Journal :
- BioMed Research International
- Accession number :
- edsair.doi.dedup.....e8333e8bc86df4088c6fb65ef717dd36