ArticleJournal of pharmacy & bioallied sciences
Sinapic acid attenuates cisplatin-induced nephrotoxicity through peroxisome proliferator-activated receptor gamma agonism in rats.
Article in Journal of pharmacy & bioallied sciences. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- Sinapic acid attenuated nephrotoxicity against Cyclophosphamide in mice model: A histochemical, immunohistochemical and histopathological evaluation.Iranian journal of basic medical sciences · 2025Article
- Sinapic acid alleviates 5-fluorouracil-induced nephrotoxicity in rats via Nrf2/HO-1 signalling.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023Article
- Protective effect of spore oil-functionalized nano-selenium system on cisplatin-induced nephrotoxicity by regulating oxidative stress-mediated pathways and activating immune response.Journal of nanobiotechnology · 2023Article
- Sinapis Semen: A review on phytochemistry, pharmacology, toxicity, analytical methods and pharmacokinetics.Frontiers in pharmacology · 2023Review
- Nephroprotective effect of polyphenol-rich extract of3 Biotech · 2022Article
- Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity.International journal of molecular sciences · 2022Review
- Sinapic acid restores blood parameters, serum antioxidants, and liver and kidney functions in obesity.Journal of diabetes and metabolic disorders · 2022Article
- Sinapic Acid Attenuated Cardiac Remodeling After Myocardial Infarction by Promoting Macrophage M2 Polarization Through the PPARγ Pathway.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimThe aim of this study was to investigate the involvement of peroxisome proliferator-activated receptor gamma (PPAR-γ) in renal protection offered by sinapic acid in cisplatin-induced nephrotoxicity in male rats. MATERIALS AND
methodsNephrotoxicity was induced by single dose of cisplatin (5 mg/kg, intraperitoneal [i.p.]) in rats. Cisplatin-induced nephrotoxicity was assessed by measuring serum creatinine, creatinine clearance, urea, uric acid, potassium, magnesium levels, fractional excretion of sodium, and microproteinuria in rats. Superoxide anion generation, thiobarbituric acid reactive substances, myeloperoxidase activity, and reduced glutathione levels were measured to assess oxidative stress in renal tissues. Hematoxylin and eosin stain showed renal histological changes.
resultsThe significant changes in serum and urinary parameters, elevated oxidative stress, and renal histological changes established the induction of nephrotoxicity. Sinapic acid treatment (20 and 40 mg/kg, orally [p.o.]) provides dose-dependent and significant (
conclusionIt is concluded that PPAR-γ agonism serves as one of the mechanisms in sinapic acid-mediated renoprotection.
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