ArticleScientific reports2025
Canagliflozin alleviates acetaminophen-induced renal and hepatic injury in mice by modulating the p-GSK3β/Fyn-kinase/Nrf-2 and p-AMPK-α/STAT-3/SOCS-3 pathways.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Sweet relief: exploring mechanisms and therapeutic approaches of sodium-glucose cotransporter-2 inhibitors in cardiovascular-kidney metabolic syndrome.Cardiovascular diabetology · 2026Review
- The SGLT2i "canagliflozin" and the DPP-4i "sitagliptin" mitigate hypertensive nephropathy in adult male rats by modulating the Ang II/RAGE/Nox4/NLRP3 cascade.Frontiers in physiology · 2026Article
- Sesamin protects against Acetaminophen-induced nephrotoxicity by suppressing HMOX1-mediated apoptosis and ferroptosis.Redox report : communications in free radical research · 2025Article
- Paracetamol Induces Apoptosis, Reduces Colony Formation, and Increases PTPRO Gene Expression in Human Embryonic Kidney HEK 293 Cells.Journal of biochemical and molecular toxicology · 2025Article
- Beyond glycemic control: the cardiac and hepatic benefits of SGLT2 and DPP-4 inhibitors in mitigating chronic cadmium-induced inflammation, oxidative/nitrative stress, apoptosis and fibrosis.Frontiers in physiology · 2025Article
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Abstract
Despite the fact that canagliflozin (Cana), a sodium-glucose cotransporter 2 inhibitor, is an anti-diabetic medication with additional effects on the kidney, there is limited experimental data to deliberate its hepato-reno-protective potentiality. Acetaminophen (APAP) overdose remains one of the prominent contributors to hepato-renal damage.
aimOur study assessed the novel effect of Cana against APAP-induced toxicities. MAIN
methodsmice were randomized into five groups: negative control, Cana KEY
findingsPre-treatment with Cana ameliorated hepatic and renal functions, whereas, on the molecular levels, Cana promoted hepatic/renal P-AMP-activated protein kinase-α/ protein kinase B (p-Akt)/Glycogen synthase kinase (p-GSK3β) protein expression. Alternatively, Cana dampened the expression of STAT-3 and Fyn-kinase genes with a subsequent increase in the contents of suppressor of cytokine signaling (SOCS)-3 and also boosted the contents of the nuclear factor erythroid related factor 2 (Nrf-2)/heme oxygenase (HO)-1/ NADPH quinone oxidoreductase (NQO)-1 axis. The crosstalk between these paths ameliorated the APAP-induced hepatorenal structural alterations. SIGNIFICANCE: Cana hepatorenal protective impact was provoked partly through modulating p-AMPK-α /SOCS-3/STAT-3 and GSK3β/Fyn-kinase signaling for its anti-inflammatory and antioxidant effects.
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