ArticleToxicology reports2026
L-carvone protects against myoglobinuric acute tubular necrosis via inhibition of NF-κB and caspase-dependent apoptotic pathways.
Article in Toxicology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Molecular Targets and Biological Activities of Carvone: An Evidence-Graded Review.Molecules (Basel, Switzerland) · 2026Review
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute kidney injury (AKI) secondary to rhabdomyolysis is a life-threatening clinical condition characterized by oxidative stress, inflammation, and tubular cell apoptosis. Effective pharmacological treatments targeting these pathophysiological cascades remain limited. Objective: This study aimed to investigate the nephroprotective effects of the natural monoterpene L-carvone in a murine model of glycerol-induced rhabdomyolysis-associated AKI. Methods: Fifty male BALB/c mice were assigned to five groups (n = 10/group): control, rhabdomyolysis (50% glycerol, 10 mL/kg), and three groups receiving prophylactic oral L-carvone (25, 50, or 100 mg/kg) for five days prior to glycerol administration. Renal function was evaluated via blood urea nitrogen (BUN), creatinine, and myoglobin. Tubular injury (KIM-1, NGAL), inflammatory gene expression (IL-1β, TNF-α, NF-κB), apoptotic protein expression (BAX, BCL-2, caspase-8, cleaved caspase-3), and renal histopathology were analyzed. Results: L-carvone pretreatment significantly lowered serum BUN, creatinine, and myoglobin levels compared to the untreated rhabdomyolysis group. Furthermore, L-carvone markedly reduced the expression of tubular injury biomarkers KIM-1 and NGAL. RT-qPCR analysis demonstrated that L-carvone substantially decreased mRNA levels of pro-inflammatory mediators IL-1β, TNF-α, and NF-κB. Western blot analysis revealed a strong anti-apoptotic shift, characterized by decreased BAX, caspase-8, and cleaved caspase-3, alongside significantly increased BCL-2. These molecular improvements strongly correlated with significantly preserved renal histopathological architecture. Conclusion: L-carvone provides robust renal protection against glycerol-induced rhabdomyolysis by attenuating key inflammatory and apoptotic signaling pathways. These preclinical findings highlight its therapeutic potential as a promising candidate for the management of rhabdomyolysis-associated AKI.
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