Literature DB >> 31655538

The effect of N-acetylcysteine on inflammation and oxidative stress in cisplatin-induced nephrotoxicity: a rat model

Inayet Güntürk, Cevat Yazici, Sema Kader Köse, Fatma Dağli, Bilal Yücel, Arzu Hanim Yay.   

Abstract

Background/Aim: Cisplatin is a highly effective chemotherapeutic agent used in the treatment of solid organ cancers. Besides its chemotherapeutic effectiveness, cisplatin administration is associated with numerous side effects. Of those, the most clinically significant and common effect is nephrotoxicity. Recent studies reported that oxidative stress and inflammation are probably the most important mechanisms that contribute to the nephrotoxicity. N-acetylcysteine (NAC) is an antioxidant and antiinflammatory agent. In the present study, the effects of NAC on cisplatin-induced nephrotoxicity were investigated. Materials and methods: Rats were divided into four groups each including eight rats: CONT, NAC-250, CP, and CP+NAC. Rats in experimental groups were treated intraperitoneally (i.p.) with a single dose of cisplatin (10 mg/kg body weight) and i.p. with NAC (250 mg/kg body weight) for three consecutive days. Nephrotoxicity was determined by plasma BUN and creatinine levels. In tissue samples, myeloperoxidase (MPO), nuclear factor-kappa B (NF-kB), high mobility group box-1 (HMGB-1), total oxidant status (TOS), and total antioxidant status (TAS) levels were measured. Kidneys were analyzed histopathologically as well.
Results: It was revealed that cisplatin was not effective on MPO, HMGB-1 and NF-kB levels but did increase TOS levels and decrease TAS levels in tissue samples. Interestingly, NAC elevated MPO and HMGB-1 levels significantly. Nevertheless, NAC ameliorated histological and functional changes in kidney tissues.
Conclusion: It is suggested that inflammation has a limited effect on cisplatin nephrotoxicity in this experimental design, and, as reflected by decreased BUN and creatinine levels, NAC can be used as an additional therapeutic agent in standard cisplatin treatment protocols. This work is licensed under a Creative Commons Attribution 4.0 International License.

Entities:  

Keywords:  N-acetylcysteine; Rats; cisplatin; inflammation; oxidative stress

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Year:  2019        PMID: 31655538     DOI: 10.3906/sag-1903-225

Source DB:  PubMed          Journal:  Turk J Med Sci        ISSN: 1300-0144            Impact factor:   0.973


  4 in total

1.  Possible protective activity of n-acetyl cysteine against cisplatin‑induced hepatotoxicity in rats.

Authors:  Özlem Coşkun; Özlem Öztopuz; Başak Büyük
Journal:  Mol Biol Rep       Date:  2021-01-13       Impact factor: 2.316

2.  N-Acetylcysteine (NAC) Inhibits Synthesis of IL-18 in Macrophage by Suppressing NLRP3 Expression to Reduce the Production of IFN-γ from NK Cells.

Authors:  Xiaopeng Liu; Xufeng Lu; Zhixiong Hu
Journal:  Comput Math Methods Med       Date:  2021-12-03       Impact factor: 2.238

3.  TRPA1 promotes cisplatin-induced nephrotoxicity through inflammation mediated by the MAPK/NF-κB signaling pathway.

Authors:  Jinyan Yuan; Xiao Liang; Wei Zhou; Jing Feng; Zhenyang Wang; Shaoxian Shen; Xin Guan; Liangbin Zhao; Fei Deng
Journal:  Ann Transl Med       Date:  2021-10

4.  CdSe/ZnS quantum dots exhibited nephrotoxicity through mediating oxidative damage and inflammatory response.

Authors:  Xiuli Li; Huiwu Zhang; Fuyun Sun
Journal:  Aging (Albany NY)       Date:  2020-11-16       Impact factor: 5.682

  4 in total

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