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Isorhamnetin Protects Against Organophosphate-Induced Cardiac Damage in Wistar Rats Through Redox Balance and
Yousra Bseiso1, Badriyah S Alotaibi2, Alaa A A Aljabali3
1Department of Biology and Biotechnology, Faculty of Science, The Hashemite University, Zarqa, Jordan.
Background:
Chlorpyrifos (CPF) triggers cardiotoxicity associated with oxidative stress, inflammation and apoptosis. This study investigated whether isorhamnetin, a chemically defined flavonol (3'-O-methylquercetin, C16H12O7, purity ≥ 98%), could mitigate CPF-induced myocardial injury.
Methods:
Male Wistar rats were randomly divided into control, isorhamnetin, CPF and CPF + isorhamnetin groups. Cardiac biomarkers, oxidative/antioxidant status, and inflammatory and apoptotic mediators in conjunction with histopathology and Nrf2/HO-1 signalization were assessed.
Results:
CPF elevated serum cTnI, CK-MB and LDH (p < 0.001), attaining lower levels after isorhamnetin cotreatment (p < 0.001). TBARS and NO were elevated (p < 0.001), whereas GSH, SOD, catalase and GPx decreased (p < 0.001) after CPF exposure; these indices were reverted with isorhamnetin. CPF increased the expression levels of NF-κB p65, TNF-α, IL-6 and IL-1β proteins and decreased that of IL-10 (p < 0.001), whereas isorhamnetin offset these effects (p < 0.001). Apoptosis was apparent with high Bax and caspase-3 and low Bcl-2 (p < 0.001); all were ameliorated by isorhamnetin. Histopathological alterations caused by CPF were ameliorated. CPF downregulated the expression and activity of Nrf2/HO-1 (p < 0.001), but this pathway was significantly induced by isorhamnetin (p < 0.001).
Conclusions:
Isorhamnetin alleviates CPF-induced cardiotoxicity by restoring redox balance and modulating inflammatory and apoptotic pathways through Nrf2/HO-1 signalling.
