Cisplatin induced Acute Renal Failure Modeling & Pharmacodynamics Service
As one of the most reliable industry leaders, Creative Biolabs is capable of providing both chronic and acute kidney failure models induced in rats and mice. Having a group of experts and scientists who are experienced in this field, not only robust, stably validated models are quickly obtained at reasonable prices but also other new models are tailored to meet your various needs.
Side Effects of Anti-Cancer Cisplatin
Acute renal failure (ARF) is defined as a state of rapid loss of kidney function which increases concentrations of serum creatinine and urea resulting in the inability of the kidney to regulate acid-electrolyte balance, and failure to excrete fluids and waste products. Cisplatin [cis-diaminedichloroplatinum(II), CP], an inorganic chemotherapeutic agent, is broadly used for the therapy of a large spectrum of solid tumors such as ovarian, head and neck carcinomas, and germ cell tumors. Although cisplatin is a highly effective anti-cancer drug, the limitations of the long-term clinical use of CP exist due to various significant side effects, mainly nephrotoxicity.
Nephrotoxicity of Cisplatin
The nephrotoxicity of CP is a major clinical problem. In humans, high dose of cisplatin (75 mg/m2) has been used as baseline chemotherapeutic agent for the management of lung cancer. However, at this dose, significant kidney damage has been seen in patients. Pathologically, CP causes impairment of kidney function and acute renal failure through multiple mechanisms, including DNA damage, the generation of free radicals, tubulointerstitial inflammation, and apoptotic cell death. Additionally, significant interactions among these various pathways may occur in cisplatin injury. Although a number of studies have evaluated compounds as potential nephroprotectors against CP, including natural antioxidants, modulators of nitric oxide synthesis, osmotic diuretics, and cytoprotective and antiapoptotic agents, most of them were not found suitable/safe for clinical practice. Therefore, it is necessary to apply cisplatin-induced ARF models in the development and evaluation of nephroprotective agents.
Fig. 1 Histological examination of morphological changes in kidney tissues by TUNEL staining.1
Application of Cisplatin-Induced AKI models
The i.p. administration of CP at varying doses (6-40 mg/kg) will elicit renal failure in mice and rats, thus providing good in vivo models to obtain an improved understanding of the pathogenesis of CP-induced AKI, which is important to prevent AKI and improve survival for cancer patients receiving cisplatin-based treatments. Moreover, increased renal vascular resistance, as well as decreases in renal plasma flow and glomerular filtration rate (GFR), make the cisplatin nephrotoxicity an ideal model to study the early pathophysiological features of all types of AKI.
Creative Biolabs provides assessments for in vivo evaluation of nephroprotective agents which including but not limited to:
- Body Weight
- Kidney Weight
- Serum Biochemical Parameters
- Urinary Protein Analysis
- Histopathological Examination
- Immunohistochemistry
Meanwhile, Creative Biolabs also offers other types of rodent urological disease models that you might be interested in:
- Unilateral Ureter Obstruction (UUO) Model
- Thy-1 Nephritis Model
- Anti-Glomerular Basement Membrane (GBM) Nephritis Model
- 5/6 Nephrectomy Model
- Adriamycin-Induced Nephropathy (AN) Rodent Model
- Gentamicin-Induced Acute Renal Failure Model
- Glycerol-Induced Acute Renal Failure Model
- Renal Ischemia-Reperfusion (IR) Model
- Cyclophosphamide-Induced Cystitis (CYP) Model
- Lipopolysaccharide (LPS)-Induced Cystitis Model
Apart from cisplatin, Creative Biolabs is capable of using other kinds of nephrotoxic drugs to induce acute kidney failure models. For more information or a formal quote, please feel free to send us an inquiry or directly contact us.
Reference
- Chien, Liang-Hsuan, et al. "Salvianolic acid c protects against cisplatin-induced acute kidney injury through attenuation of inflammation, oxidative stress and apoptotic effects and activation of the CaMKK-AMPK-sirt1-associated signaling pathway in mouse models." Antioxidants 10.10 (2021): 1620. doi:10.3390/antiox10101620. Distributed under Open Access license CC BY 4.0. The image was modified by extracting and using the B part of the original image.
For Research Use Only.