# Sinapic acid attenuated nephrotoxicity against Cyclophosphamide in mice model: A histochemical, immunohistochemical and histopathological evaluation

**Authors:** Saeed Raoof, Shiva Rezaei, Mehryar Zargari, Mansoureh Mirzaei, Seyed Jalal Hosseinimehr, Abbasali Karimpour Malekshah, Fereshteh Talebpour Amiri

PMC · DOI: 10.22038/ijbms.2025.83903.18155 · Iranian Journal of Basic Medical Sciences · 2025-01-01

## TL;DR

Sinapic acid may help protect the kidneys from damage caused by the chemotherapy drug cyclophosphamide in mice.

## Contribution

The study demonstrates that sinapic acid reduces cyclophosphamide-induced nephrotoxicity through antioxidant and anti-inflammatory mechanisms.

## Key findings

- Sinapic acid reduced oxidative stress markers and improved kidney function in mice treated with cyclophosphamide.
- Histopathological and immunohistochemical analyses showed reduced kidney damage and inflammation in mice given sinapic acid.
- Higher doses of sinapic acid were more effective in mitigating cyclophosphamide-induced nephrotoxicity.

## Abstract

Cyclophosphamide (CP) is a chemotherapeutic drug used to treat various tumors. It causes nephrotoxicity by producing reactive oxygen species. Sinapic acid (SA) exhibits anti-oxidant, antiapoptotic, and anti-inflammatory activities at low doses as a phenylpropanoid. This study aimed to investigate the protective effects of SA on SP-induced renal injury.

Forty-eight BALB/c mice were randomly divided into control, SA (for seven consecutive days, with two doses of 5 and 10 mg/kg), CP (single dose, 200 mg/kg), and CP + SA (5 and 10 mg/kg). On the 10th day of the study, mice were examined by renal function markers (Urea and Creatinine), oxidative stress markers (MDA and GSH), histopathological, and immunohistochemical assays (caspase-3 and NF-kB kidney).

MDA levels increased and GSH levels decreased significantly in CP-treated mice. In addition, the histopathological structure of the kidney tissue in CP-treated mice showed significantly severe kidney tissue damage associated with increased urea and creatinine. The administration of SA in CP-treated mice significantly reduced serum urea and creatinine concentrations. In addition, the immunohistochemical staining of caspase- 3 and NF-kB decreased significantly in the CP + SA group compared to CP-treated mice.

Overall, our study suggests that sinapic acid, a substance with antioxidant, antiapoptotic, and anti-inflammatory properties, can be used as a complementary therapy to protect nephrotoxicity against CP.

## Linked entities

- **Proteins:** Casp3 (caspase 3), NFKB1 (nuclear factor kappa B subunit 1)
- **Chemicals:** Cyclophosphamide (PubChem CID 2907), Sinapic acid (PubChem CID 10743), MDA (PubChem CID 1614), GSH (PubChem CID 124886), Urea (PubChem CID 1176), Creatinine (PubChem CID 588)

## Full-text entities

- **Genes:** Casp3 (caspase 3) [NCBI Gene 12367] {aka A830040C14Rik, AC-3, CASP-3, CC3, CPP-32, CPP32}, Tff2 (trefoil factor 2 (spasmolytic protein 1)) [NCBI Gene 21785] {aka SP, mSP}
- **Diseases:** kidney tissue damage (MESH:D007674), inflammatory (MESH:D007249), tumors (MESH:D009369)
- **Chemicals:** Urea (MESH:D014508), MDA (MESH:D015104), SA (MESH:C073734), Creatinine (MESH:D003404), reactive oxygen species (MESH:D017382), phenylpropanoid (-), GSH (MESH:D005978), CP (MESH:D003520)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12258792/full.md

## References

30 references — full list in the complete paper: https://tomesphere.com/paper/PMC12258792/full.md

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Source: https://tomesphere.com/paper/PMC12258792