PUBLICATION

Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish

Authors
Morales Fénero, C., Padovani, B.N., do Amaral, M.A., de Barros, G.J.B., de Oliveira, I.K.X., Hiyane, M.I., Camâra, N.O.S.
ID
ZDB-PUB-210601-13
Date
2021
Source
Journal of visualized experiments : JoVE   (171): (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Acute Kidney Injury*/chemically induced
  • Animals
  • Cisplatin*/toxicity
  • Humans
  • Kidney
  • Regeneration
  • Zebrafish*
PubMed
34057433 Full text @ J. Vis. Exp.
Abstract
Cisplatin is commonly used as chemotherapy. Although it has positive effects in cancer-treated individuals, cisplatin can easily accumulate in the kidney due to its low molecular weight. Such accumulation causes the death of tubular cells and can induce the development of Acute Kidney Injury (AKI), which is characterized by a quick decrease in kidney function, tissue damage, and immune cells infiltration. If administered in specific doses cisplatin can be a useful tool as an AKI inducer in animal models. The zebrafish has appeared as an interesting model to study renal function, kidney regeneration, and injury, as renal structures conserve functional similarities with mammals. Adult zebrafish injected with cisplatin shows decreased survival, kidney cell death, and increased inflammation markers after 24 h post-injection (hpi). In this model, immune cells infiltration and cell death can be assessed by flow cytometry and TUNEL assay. This protocol describes the procedures to induce AKI in adult zebrafish by intraperitoneal cisplatin injection and subsequently demonstrates how to collect the renal tissue for flow cytometry processing and cell death TUNEL assay. These techniques will be useful to understand the effects of cisplatin as a nephrotoxic agent and will contribute to the expansion of AKI models in adult zebrafish. This model can also be used to study kidney regeneration, in the search for compounds that treat or prevent kidney damage and to study inflammation in AKI. Moreover, the methods used in this protocol will improve the characterization of tissue damage and inflammation, which are therapeutic targets in kidney-associated comorbidities.
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