Introduction to the RIRI Animal Model

Renal ischemia-reperfusion injury (RIRI) is caused by inadequate renal perfusion resulting from various etiologies and is accompanied by a cascade of cellular events, including the release of reactive oxygen species (ROS), apoptosis, necrosis, infiltration of inflammatory cells, and the release of bioactive mediators, ultimately leading to tissue damage. It is commonly observed in diverse clinical scenarios, such as various types of shock, acute renal artery occlusion, or kidney transplantation, and represents the most frequent cause of acute kidney injury (AKI) in clinical practice.

RIRI Animal Model Platform Service Advantages of Aniphe BioLab

Leveraging established renal ischemia-reperfusion injury (RIRI) modeling techniques and a comprehensive pharmacological evaluation platform, Aniphe BioLab offers end-to-end model‑based research services.

	The model system is mature. By employing standardized modeling techniques, animal models with varying degrees of injury can be established, exhibiting excellent stability and reproducibility.
	Multidimensional evaluation capability It can perform assays for a wide range of parameters, including renal function, histopathology, inflammation, oxidative stress, and apoptosis.
	The modeling approach is flexible. Users can select unilateral or bilateral ischemia, as well as varying durations of ischemia, to suit applications such as acute kidney injury, renal repair, and mechanistic studies.
	Strict standardized quality control procedures Ensuring model success rates and data reliability, thereby supporting basic research on kidney diseases and the development of innovative therapeutics.

Modeling cycle	1–2 weeks
Laboratory animals	Mice, rats, rabbits, and miniature pigs
Positive drug	Commonly used agents such as dexmedetomidine, N-acetylcysteine, edaravone, and dexamethasone serve as positive controls and exert renal protective effects by modulating inflammation, combating oxidative stress, and mitigating tubular injury.
Application areas	It is primarily used for research on acute kidney injury and the mechanisms of renal ischemia-reperfusion, screening of nephroprotective drugs, evaluation of drug efficacy, as well as preclinical studies of cell therapy and innovative therapeutic approaches.

Construction of RIRI Animal Models

Ischemia–reperfusion (bilateral renal artery clamping): By temporarily clamping both renal arteries to occlude renal blood flow, maintaining a defined period of ischemia, and then releasing the clamp to restore perfusion, this model induces ischemia–reperfusion injury in the kidney. It reliably mimics the hallmark pathological changes observed in acute kidney injury, including inflammatory responses, oxidative stress, and tubular damage, and is characterized by model stability and excellent reproducibility.

Edaravone treatment data

Renal ischemia triggers intense oxidative stress and lipid peroxidation, leading to marked tubular necrosis and pathological damage to renal tissue. Following treatment with edaravone, both reactive oxygen species accumulation and lipid oxidation products were reduced, and tubular pathology was alleviated. Statistical analysis further demonstrated significant differences compared with the ischemia‑only group (*P<0.05, *P<0.01), thereby confirming that edaravone can ameliorate ischemia‑induced acute kidney injury through its antioxidant effects.

Ischemia increases renal lipid peroxidation and exacerbates oxidative stress; edaravone exerts renoprotective antioxidant effects: in vivo, it downregulates HHE‑modified proteins and attenuates ischemia‑induced lipid oxidation–mediated injury; at the cellular level, its efficacy is concentration‑dependent, with a 10⁻⁴ mol/L dose markedly inhibiting intracellular ROS production in HKC‑8 renal tubular cells and sustaining this inhibition over time, thereby alleviating oxidative stress and conferring renal protection.