ArticleMolecular and cellular biochemistry2026
Amelioration of doxorubicin-mediated nephrotoxicity through antioxidant and anti-apoptotic mechanisms of 5,4'-dihydroxy-6,8-dimethoxy-7-O-rhamnosylflavone.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Doxorubicin (DOX), a cornerstone chemotherapeutic, induces dose-limiting nephrotoxicity through NOX-4-mediated oxidative stress, inflammatory signalling, and apoptosis, thereby compromising its long-term clinical utility. This study investigated whether 5,4'-dihydroxy-6,8-dimethoxy-7-O-rhamnosylflavone (DDR), a bioactive flavonoid, protects against chronic DOX-induced renal injury. To evaluate DDR's renoprotective efficacy and elucidate its mechanistic involvement of NOX-4, NRF2, and apoptotic pathways. Male Swiss albino mice (n = 6/group) received: control vehicle, DOX (2.5 mg/kg i.p., weekly × 6 weeks), DOX + DDR (25 or 50 mg/kg i.p., twice weekly), or DDR alone. Renal function (creatinine, urea, NGAL, KIM-1), oxidative stress markers (MDA, SOD, CAT, GSH), cytokines (pNFκB, TNF-α, IL-6, IL-1β), and protein expression (NOX-4, NRF2, BCL2, BCL-XL, Caspase-3) were quantified. Histopathology employed H&E and Masson's trichrome with semi-quantitative injury scoring. DOX induced severe nephrotoxicity (serum creatinine ↑347%, tubular injury score 14.8 ± 1.4, p < 0.001), characterized by NOX-4 overexpression, NRF2 suppression, and apoptosis (Caspase-3 ↑412%). DDR elicited dose-dependent protection; high-dose DDR restored renal function (creatinine ↓78%), normalized histopathology (score 2.8 ± 0.9, p < 0.001), suppressed NOX and reactivated NRF2, and prevented apoptosis. DDR provides potent, mechanistically defined renoprotection against DOX nephrotoxicity through multi-target modulation of oxidative, inflammatory, and apoptotic pathways. These preclinical findings support DDR's development as a clinically translatable chemotherapeutic adjuvant (Human equivalent dose: 2-4 mg/kg).
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