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The effect of anakinra to nephrotoxicity with cisplatin induced in rats: Biochemical, gene expression and
Adalet Ozcicek1, Fatih Ozcicek1, Ferda Keskin Cimen2
1Department of Internal Medicine, Faculty of Medicine, Erzincan University, Turkey.
Background:
Oxidative stress and interleukin-1 beta (IL-1β) have been reported to play a role in the pathogenesis of nephrotoxicity induced by cisplatin.
Objectives:
The objective of this study was to investigate the effect of anakinra, which is an IL-1β receptor antagonist, on cisplatin-induced nephrotoxicity in rats, through biochemical, gene expression and histopathological analyses.
Material And Methods:
The study was designed with 4 groups. For 1 week, the control group (C) and the cisplatin (Cis) group received distilled water, while the cisplatin + anakinra 50 (Cis + ANA50) group and the cisplatin + anakinra 100 (Cis + ANA100) group were intraperitoneally administered 50 mg/kg and 100 mg/kg of anakinra, respectively. The Cis, Cis + ANA50 and Cis + ANA100 groups were intraperitoneally injected with a 2.5 mg/kg dose of cisplatin for 7 days. After sacrifice, the kidney tissue of each rat was extracted for the assessment of the malondialdehyde (MDA) and total glutathione (tGSH) levels, and for gene expression analyses of IL-1β. The kidney tissues were histopathologically evaluated. Statistical analyses of the data were performed using one-way analysis of variance (ANOVA).
Results:
The administration of cisplatin (the Cis group) yielded a higher level of MDA (4.75 ±0.25 nmol/mL; p < 0.001) and lower levels of tGSH (1.80 ±0.35 mg/L; p < 0.001) compared to other groups. Cisplatin also increased IL-1β gene expression (6.33 ±0.27 gene expression levels; p < 0.001) compared to other groups. The impact of anakinra on the MDA and tGSH levels, and on IL-1β gene expression induced by cisplatin was observed as a reversal of these findings (p < 0.05). Anakinra better prevented an increase of the levels of MDA and IL-1β at a dose of 100 mg/kg compared to a 50 mg/kg dose.
Conclusions:
Anakinra prevents oxidative kidney damage induced by cisplatin, in a dose-dependent manner. This result suggests that anakinra may be useful in the treatment of cisplatin-induced kidney damage.
Insights
Anakinra, an IL-1β receptor antagonist, prevents cisplatin-induced kidney damage by reducing oxidative stress. This suggests anakinra may be a potential treatment for nephrotoxicity.
Area of Science:
- Nephrology
- Pharmacology
- Toxicology
Background:
- Cisplatin chemotherapy can cause kidney damage (nephrotoxicity).
- Oxidative stress and elevated interleukin-1 beta (IL-1β) are implicated in cisplatin-induced nephrotoxicity.
- IL-1β receptor antagonists may offer a protective effect.
Purpose of the Study:
- To investigate the protective effects of anakinra, an IL-1β receptor antagonist, against cisplatin-induced nephrotoxicity in a rat model.
- To evaluate anakinra's impact through biochemical, gene expression, and histopathological analyses.
Main Methods:
- Rats were divided into four groups: control, cisplatin, cisplatin + anakinra (50 mg/kg), and cisplatin + anakinra (100 mg/kg).
- Cisplatin was administered to induce nephrotoxicity.
- Kidney tissues were analyzed for malondialdehyde (MDA), total glutathione (tGSH), and IL-1β gene expression.
- Histopathological evaluation of kidney tissues was performed.
Main Results:
- Cisplatin significantly increased MDA and IL-1β levels while decreasing tGSH levels.
- Anakinra administration reversed these cisplatin-induced changes in a dose-dependent manner.
- The 100 mg/kg anakinra dose showed a stronger protective effect against MDA and IL-1β elevation.
Conclusions:
- Anakinra effectively prevents cisplatin-induced oxidative kidney damage.
- The protective effect of anakinra is dose-dependent.
- Anakinra shows potential as a therapeutic agent for managing cisplatin-induced nephrotoxicity.
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