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In terms of oxidative stress, CVB-D was found to inhibit oxidative stress by activating the Nrf2 signaling pathway, inhibit cardiomyocyte scorching by suppressing NLRP3 expression, and improve cardiac function and survival in rats with diabetic cardiomyopathy (68, 69), protect rat aortic endothelial cells from hypoxia and enhance NO release from endothelial cells (70), alleviate adriamycin-induced myocardial oxidative damage (which is mainly manifested by lipid peroxidation and protein carbonylation and reduced ratio of glutathione (GSH) to oxidized glutathione (GSSG)

[62] explored the therapeutic potential of an immunoglobulin G (IgG) monoclonal antibody with neutralizing specificity for MMP-9, which significantly attenuated BBB disruption in the stroke model

This imbalance has been implicated in the pathogenesis of inflammation, accelerated aging, and chronic diseases

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