ArticleJournal of biochemical and molecular toxicology2025
Protective Effects of Chrysin Against Diclofenac-Induced Nephrotoxicity in Rats via Attenuation of Oxidative Stress, Apoptosis and Endoplasmic Reticulum Stress.
Article in Journal of biochemical and molecular toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Rutin attenuates Tramadol-induced lung injury in rats by modulating oxidative stress, inflammation, endoplasmic reticulum stress, and apoptosis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Chrysin mitigates ciprofloxacin-induced nephrotoxicity: associations with notch/HES1 signaling, inflammation, and a ferroptosis-related molecular signature.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The effects of Palbociclib and Ferulic acid combination on cellular processes in breast cancer.Discover oncology · 2026Article
- A natural nephroprotective adjuvant for cancer chemotherapy: Rosmarinic acid disrupts IL-17 A-Ferroptosis coupling in Ifosfamide-induced renal injury.Medical oncology (Northwood, London, England) · 2026Article
- Protective Role of Chrysin against Mercury Chloride-Induced Testicular Damage via Oxidative Stress, Inflammation, Apoptosis, Endoplasmic Reticulum Stress, and Autophagy Pathways.Biological trace element research · 2026Article
- Hesperidin and Its Polylactic-ACS omega · 2025Article
- Chrysin, a glycolytic inhibitor, modulates redox homeostasis during aging via a potent calorie restriction mimetic effect in male wistar rats.Biogerontology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Diclofenac (DCL) is a broadly prescribed non-steroidal anti-inflammatory drug (NSAID) for pain management and has been linked to nephrotoxicity despite its therapeutic benefits. This study provides new insights into the palliative impacts of chrysin (CH) against DCL-induced kidney damage by modulating oxidative injury, endoplasmic reticulum (ER) stress and apoptosis. The rats were divided into five groups: the control group (Group 1), CH-only group (50 mg/kg, Group 2), DCL-only group (50 mg/kg, Group 3), DCL + CH (25 mg/kg, Group 4), and DCL + CH (50 mg/kg, Group 5). DCL injection led to significant renal damage marked by elevated serum urea, creatinine and malondialdehyde (MDA) levels, reduced glutathione (GSH) concentration, and decreased activities of antioxidant enzymes (glutathione peroxidase, superoxide dismutase and catalase). The mRNA expression levels of Ho-1 and Nrf2 were also suppressed. Additionally, DCL treatment triggered apoptosis as evidenced by increased expression of Bax and caspase-3 alongside decreased Bcl-2 expression. Furthermore, DCL induced ER stress was confirmed by upregulation of Perk, Ire1, Atf-6, and Grp78 transcription levels. Also, it was demonstrated that DCL treatment upregulated Mmp2 and Mmp9 levels. Treatment with CH significantly mitigated these adverse effects suggesting that CH effectively protects DCL-induced kidney toxicity by targeting multiple pathways. In summary, this study highlights the importance of CH as a promising therapeutic agent for alleviating kidney damage associated with DCL toxicity.
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Registered trials
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