# The renoprotective effects of tadalafil on ischemia–reperfusion injury during partial nephrectomy in an animal model

**Authors:** Eun Hye Lee, Eun Sang Yoo, Bo Hyun Yoon, Minji Jeon, Tae Gyun Kwon, Bum Soo Kim, Yun-Sok Ha, Man-Hoon Han, Phil Hyun Song, Jae-Wook Chung

PMC · DOI: 10.1186/s12882-025-04265-2 · BMC Nephrology · 2025-07-01

## TL;DR

Tadalafil protects kidneys from injury during partial nephrectomy by reducing inflammation and oxidative stress in a rat model.

## Contribution

Tadalafil was shown to reduce oxidative stress and inflammation markers and protect against glomeruli loss during ischemia–reperfusion injury.

## Key findings

- Tadalafil preserved renal function by preventing viable glomeruli loss after ischemia–reperfusion injury.
- Tadalafil reduced oxidative stress markers like inducible NOS and myeloperoxidase.
- Inflammation-related genes such as TNF-α, IL-1β, and IL-6 were significantly suppressed by tadalafil.

## Abstract

Although 25 min is the reported safe partial nephrectomy time for warm ischemia, acute kidney injury occurs even with arterial ligation within 25 min, causing serious complications in patients with chronic renal disease. Various drugs have been studied but evidence of their effectiveness and safety is insufficient. This study investigated the renoprotective function of tadalafil.

A rat model of partial nephrectomy was treated orally with tadalafil for 14 days before ischemic–reperfusion (IR) injury. Blood and kidney samples were collected for biochemical and molecular analyses 24 h after IR injury. The levels of serum blood urea nitrogen, creatinine, and urine kidney injury molecule-1 were analyzed, while kidney tissues were used for qPCR and histological analysis.

Although effects on blood urea nitrogen and creatine levels were not observed, tadalafil preserved renal function by suppressing the decrease of viable glomeruli, indicating it protected kidneys from IR injury-induced glomeruli loss. Tadalafil effectively reduced the expression of the oxidative stress markers, inducible NOS, endothelial NOS, and myeloperoxidase, and significantly suppressed the expression of inflammation-related genes like TNF-α, IL-1β, IL-6, CD4, and CD8.

Tadalafil inhibits oxidative stress and inflammation, and protects from glomeruli loss during ischemic–reperfusion damage in a rat model of partial nephrectomy.

Not applicable.

The online version contains supplementary material available at 10.1186/s12882-025-04265-2.

## Linked entities

- **Genes:** NOS2 (nitric oxide synthase 2) [NCBI Gene 4843], NOS3 (nitric oxide synthase 3) [NCBI Gene 4846], MPO (myeloperoxidase) [NCBI Gene 4353], TNF (tumor necrosis factor) [NCBI Gene 7124], IL1B (interleukin 1 beta) [NCBI Gene 3553], IL6 (interleukin 6) [NCBI Gene 3569], CD4 (CD4 molecule) [NCBI Gene 920], CD8A (CD8 subunit alpha) [NCBI Gene 925]
- **Chemicals:** tadalafil (PubChem CID 110635)
- **Species:** Rattus norvegicus (taxon 10116)

## Full-text entities

- **Genes:** Il6 (interleukin 6) [NCBI Gene 24498] {aka ILg6, Ifnb2}, Nos3 (nitric oxide synthase 3) [NCBI Gene 24600] {aka eNos}, Tnf (tumor necrosis factor) [NCBI Gene 24835] {aka RATTNF, TNF-alpha, Tnfa}, Cd4 (Cd4 molecule) [NCBI Gene 24932] {aka W3/25, p55}, Mpo (myeloperoxidase) [NCBI Gene 303413], Havcr1 (hepatitis A virus cellular receptor 1) [NCBI Gene 286934] {aka KIM-1, Kim1}, Nos2 (nitric oxide synthase 2) [NCBI Gene 24599] {aka Nos2a, iNos}
- **Diseases:** reperfusion damage (MESH:D015427), inflammation (MESH:D007249), ischemic (MESH:D002545), ischemia (MESH:D007511)
- **Chemicals:** creatine (MESH:D003401), Tadalafil (MESH:D000068581), creatinine (MESH:D003404)
- **Species:** Rattus norvegicus (brown rat, species) [taxon 10116]

## Full text

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## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12220080/full.md

## References

6 references — full list in the complete paper: https://tomesphere.com/paper/PMC12220080/full.md

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Source: https://tomesphere.com/paper/PMC12220080