ArticleMetabolites2022
Upregulation of Nrf2/HO-1 Signaling and Attenuation of Oxidative Stress, Inflammation, and Cell Death Mediate the Protective Effect of Apigenin against Cyclophosphamide Hepatotoxicity.
Article in Metabolites, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Cardioprotective role of vincamine in cyclophosphamide-induced cardiotoxicity through modulation of AMPK/SIRT1, PI3K/Akt, and MAPK pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Review
- SP-3 Ameliorates Established Cyclophosphamide-Induced Liver Injury and Is Associated with PPAR-Related Transcriptional and Lipid-Metabolic Changes.International journal of molecular sciences · 2026Article
- Flavonoids as Nutraceuticals to Treat Inflammatory Diseases: Focusing on Quercetin, Kaempferol, Luteolin, Apigenin, Epicatechin and Their Effects on Hepatic, Nervous, and Pulmonary Systems.Foods (Basel, Switzerland) · 2026Review
- Effects of quercetin-loaded nanoselenium on spermatogenesis in a mouse model of cyclophosphamide-induced testicular damage.Clinical and experimental reproductive medicine · 2026Article
- Diacerein mitigates cisplatin-induced testicular toxicity in rats; Role of Nrf2/ HO-1, NF-κB/caspase-3 and NLRP3/ASC/Caspase-1 signaling pathways.Molecular biology reports · 2026Article
- Article
- Modulation of AMPK/SIRT1 signaling by piribedil attenuates cyclophosphamide-induced nephrotoxicity via PI3K/Akt, MAPKs, and TLR4/NLRP3 pathways with regulation of KIM-1/NGAL.Naunyn-Schmiedeberg's archives of pharmacology · 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
- Unraveling chemotherapy-evoked hepatic dysfunction: a deep dive into cyclophosphamide-related liver injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Targeting AMPK with ivabradine attenuates cyclophosphamide-induced hepatotoxicity: Crosstalk with MAPK, JAK1/STAT3, and PI3K/Akt pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Targeting SIRT-1/AMPK/Nrf2 Signaling Pathway by Tenofovir Protected Against Cyclophosphamide-Induced Nephrotoxicity and Cardiotoxicity in Rats.Pharmaceutics · 2025Article
- Article
- Alfalfa (Medicago sativa) and neurodegeneration: mechanistic insights into oxidative stress, inflammation, and neuronal survival pathways.Molecular biology reports · 2025Review
- L-arginine administration exacerbates myocardial injury in diabeticsWorld journal of diabetes · 2025Article
- Review
- Hepatoprotective and antioxidant effects ofInternational journal of biochemistry and molecular biology · 2025Article
- Rosmarinic acid protects against cyclophosphamide-induced hepatotoxicity via inhibition of oxidative stress, inflammation, and apoptosis and upregulation of Nrf2 in mice.Journal of molecular histology · 2024Article
- The Therapeutic Mechanisms of Honey in Mitigating Toxicity from Anticancer Chemotherapy Toxicity: A Review.Journal of xenobiotics · 2024Review
- Review
Corrections and comments
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Authors and funding
13 authors at 8 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver injury is among the adverse effects of the chemotherapeutic agent cyclophosphamide (CP). This study investigated the protective role of the flavone apigenin (API) against CP-induced liver damage, pointing to the involvement of Nrf2/HO-1 signaling. Rats were treated with API (20 and 40 mg/kg) for 15 days and received CP (150 mg/kg) on day 16. CP caused liver damage manifested by an elevation of transaminases, alkaline phosphatase (ALP), and lactate dehydrogenase (LDH), and histological alterations, including granular vacuolation, mononuclear cell infiltration, and hydropic changes. Hepatic reactive oxygen species (ROS), malondialdehyde (MDA), and nitric oxide (NO) were increased and glutathione (GSH) and antioxidant enzymes were decreased in CP-administered rats. CP upregulated the inflammatory markers NF-κB p65, TNF-α, IL-6, and iNOS, along with the pro-apoptotic Bax and caspase-3. Pre-treatment with API ameliorated circulating transaminases, ALP, and LDH, and prevented histopathological changes in CP-intoxicated rats. API suppressed ROS, MDA, NO, NF-κB p65, iNOS, inflammatory cytokines, oxidative DNA damage, Bax, and caspase-3 in CP-intoxicated rats. In addition, API enhanced hepatic antioxidants and Bcl-2 and boosted the Nrf2 and HO-1 mRNA abundance and protein. In conclusion, API is effective in preventing CP hepatotoxicity by attenuating oxidative stress, the inflammatory response, and apoptosis. The hepatoprotective efficacy of API was associated with the upregulation of Nrf2/HO-1 signaling.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.