Iranian journal of basic medical sciences · 2026
Exploring the renoprotective effects of umbelliferone in rats subjected to ischemia/reperfusion injury.
СтатьяНазвание и аннотация: Перевод в очереди
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Baser Omer Faruk, Guraslan Ali, Sarikaya Bengul Ozdemi̇r, Karamese Selina Aksak, Bayram Pinar
Аннотация
OBJECTIVES: Renal ischemia/reperfusion (IR) injury is a major cause of acute kidney injury, driven by oxidative stress, inflammation, and apoptosis. This study investigated the dose-dependent renoprotective effects of umbelliferone, a coumarin derivative, in a rat model of renal IR injury.
MATERIALS AND METHODS: Thirty female Wistar rats were randomly assigned to five groups (n=6): Control, Sham, IR, IR+U50 mg/kg, and IR+U100 mg/kg. Serum cytokines (TNF-α, IL-1β, IL-6, IL-10, IL-15, IL-18, TGF-β) were measured by ELISA; renal oxidative stress markers (MDA, GSH, NO) by biochemical assays; NF-κB by immunohistochemistry; and Bax, Bcl-2, NF-κB, NRF2, P2X7, and TNF-α gene expression by RT-qPCR.
RESULTS: IR injury significantly increased pro-inflammatory cytokines, including IL-6 (15.03→25.11 ng/mL), TNF-α (55.63→70.62 ng/l), and IL-1β; elevated MDA (1.90→9.64 nmol/g) and NO (4.02→8.58 µM); and depleted GSH (9.81→1.86 nmol/g)(all P<0.001). Renal Bax, NF-κB, P2X7, and TNF-α expression and NF-κB immunoreactivity were increased, whereas NRF2 was decreased (P<0.001). Umbelliferone, particularly at 100 mg/kg, significantly reversed these changes, lowering IL-6 (15.12 ng/ml), TNF-α (57.55 ng/l), MDA (3.21 nmol/g), and NO (4.45 µM), restoring GSH (4.27 nmol/g) (P<0.001 vs IR), attenuating Bax, NF-κB, P2X7, and TNF-α expression, and partially restoring NRF2.
CONCLUSION: In this preclinical model, umbelliferone was associated with dose-dependent renoprotective effects against acute renal IR injury, attenuating oxidative stress, inflammation, and apoptosis. Further functional and mechanistic studies are needed before its therapeutic potential can be established.
MATERIALS AND METHODS: Thirty female Wistar rats were randomly assigned to five groups (n=6): Control, Sham, IR, IR+U50 mg/kg, and IR+U100 mg/kg. Serum cytokines (TNF-α, IL-1β, IL-6, IL-10, IL-15, IL-18, TGF-β) were measured by ELISA; renal oxidative stress markers (MDA, GSH, NO) by biochemical assays; NF-κB by immunohistochemistry; and Bax, Bcl-2, NF-κB, NRF2, P2X7, and TNF-α gene expression by RT-qPCR.
RESULTS: IR injury significantly increased pro-inflammatory cytokines, including IL-6 (15.03→25.11 ng/mL), TNF-α (55.63→70.62 ng/l), and IL-1β; elevated MDA (1.90→9.64 nmol/g) and NO (4.02→8.58 µM); and depleted GSH (9.81→1.86 nmol/g)(all P<0.001). Renal Bax, NF-κB, P2X7, and TNF-α expression and NF-κB immunoreactivity were increased, whereas NRF2 was decreased (P<0.001). Umbelliferone, particularly at 100 mg/kg, significantly reversed these changes, lowering IL-6 (15.12 ng/ml), TNF-α (57.55 ng/l), MDA (3.21 nmol/g), and NO (4.45 µM), restoring GSH (4.27 nmol/g) (P<0.001 vs IR), attenuating Bax, NF-κB, P2X7, and TNF-α expression, and partially restoring NRF2.
CONCLUSION: In this preclinical model, umbelliferone was associated with dose-dependent renoprotective effects against acute renal IR injury, attenuating oxidative stress, inflammation, and apoptosis. Further functional and mechanistic studies are needed before its therapeutic potential can be established.