ArticleAmerican journal of translational research2025
Klotho mitigates diquat-induced myocardial injury in rats by activating Nrf2/ARE-mediated suppression of oxidative stress.
Article in American journal of translational research, 2025. 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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4 authors.
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Abstract
objectivesDiquat (DQ) induces severe cardiotoxicity through oxidative stress, yet no specific antidote is currently available. Klotho, a known agonist of nuclear factor erythroid 2-related factor 2 (Nrf2), exerts antioxidative effects in various diseases. However, its role in DQ-induced myocardial injury remains undefined.
methodsAcute myocardial injury was induced in rats by intragastric DQ administration, followed by treatment with recombinant Klotho protein. Myocardial histopathology, oxidative stress markers, and components of the Nrf2/antioxidant response elements (ARE) pathway - including Nrf2, heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase 1 (NQO1) - were evaluated. Additionally, DQ-exposed H9c2 cardiomyocytes were treated with Klotho or the Nrf2 inhibitor ML385. cell viability, apoptosis, oxidative stress markers, and Nrf2 pathway protein expression were evaluated.
resultsDQ administration induced significant oxidative stress and upregulated mRNA levels (2-3-fold; all
conclusionKlotho mitigates DQ-induced myocardial injury in rats by activating Nrf2/ARE signaling pathway and suppressing oxidative stress.
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