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Additionally, O 2 can react with nitric oxide (NO) to generate excessive ONOO, activating caspases, causing lipid peroxidation, and leading to either apoptosis or necrosis [49]

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For example, the activation of inflammasomes, especially the NLRP3 inflammasome, leads to endothelial dysfunction, plaque formation, and myocardial injury by inducing the release of pro-inflammatory cytokines such as IL-1, IL-18, and IL-6 ( 5.1 The anti-inflammatory effect in atherosclerosis Silybin has been shown to reduce the inflammatory response in atherosclerotic lesions, with its core mechanism involving the direct inhibition of key pro-inflammatory signaling pathways