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Under hyperglycemia, lipids, proteins, and nuclear acids can form advanced glycation end products, interact with the corresponding receptor and finally trigger the activation of inflammation, oxidative stress, and mitochondrial dysfunction, which ultimately induces neuronal injury ( 3.1 In vitro evidence Qi et al

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Sulforaphane attenuation of type 2 diabetes-induced aortic damage was associated with the upregulation of Nrf2 expression and function

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In patients with resistant hypertension, 26.9% were able to decrease their blood pressure medication while taking semaglutide, compared to only 3% in the placebo group [5]

This might be attributed to the impact of the HLB values of examined edge activators