ArticleIranian journal of basic medical sciences2023
Sinapic acid attenuates cyclophosphamide-induced liver toxicity in mice by modulating oxidative stress, NF-κB, and caspase-3.
Article in Iranian journal of basic medical sciences, 2023. 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, 5 citations in OpenAlex.
- From brain to body: sinapic acid prevents multi-organ damage post-traumatic brain injury in mice.Metabolic brain disease · 2026Article
- Buspirone combats cyclophosphamide-provoked hepatotoxicity in rats via activation of AMPK/Nrf2/HO-1 and suppression of NF-κB p65 /NLRP3 inflammasome pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Sinapic Acid Ameliorates Cadmium-Induced Hepatotoxicity: Modulation of Oxidative Stress, Inflammation, and Apoptosis.Biomedicines · 2025Article
- Verbenone prevents cyclophosphamide-induced oxidative stress, inflammation, fibrosis, and cellular changes in the kidneys of Swiss albino mice by targeting NF-ĸB/TGF-β signaling pathways.Iranian journal of basic medical sciences · 2025Article
- Effects of Zofenopril and Thymoquinone in Cyclophosphamide-Induced Urotoxicity and Nephrotoxicity in Rats; The Value of Their Anti-Inflammatory and Antioxidant Properties.Journal of inflammation research · 2025Article
- Protective potential of pterostilbene against cyclophosphamide-induced nephrotoxicity and cystitis in rats.International urology and nephrology · 2023Article
- Ferulic, Sinapic, 3,4-Dimethoxycinnamic Acid and Indomethacin Derivatives with Antioxidant, Anti-Inflammatory and Hypolipidemic Functionality.Antioxidants (Basel, Switzerland) · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objectives: Cyclophosphamide (CP) as an antineoplastic drug is widely used in cancer patients, and liver toxicity is one of its complications. Sinapic acid (SA) as a natural phenylpropanoid has anti-oxidant, anti-inflammatory, and anti-cancer properties. Materials and Methods: The purpose of the current study was to determine the protective effect of SA versus CP-induced liver toxicity. In this research, BALB/c mice were treated with SA (5 and 10 mg/kg) orally for one week, and CP (200 mg/kg) was injected on day 3 of the study. Oxidative stress markers, serum liver-specific enzymes, histopathological features, caspase-3, and nuclear factor kappa-B cells were then checked. Results: CP induced hepatotoxicity in mice and showed structural changes in liver tissue. CP significantly increased liver enzymes and lipid peroxidation, and decreased glutathione. The immunoreactivity of caspase-3 and nuclear factor kappa-B cells was significantly increased. Administration of SA significantly maintained histochemical parameters and liver function enzymes in mice treated with CP. Immunohistochemical examination showed SA reduced apoptosis and inflammation. Conclusion: The data confirmed that SA with anti-apoptotic, anti-oxidative, and anti-inflammatory activities was able to preserve CP-induced liver injury in mice.
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