Leonurine Ameliorates Oxidative Stress and Insufficient Angiogenesis by Regulating the PI3K/Akt-eNOS Signaling Pathway in H<sub>2</sub>O<sub>2</sub>-Induced HUVECs

<div>H<sub>2</sub>O<sub>2</sub> can induce the expression of apoptotic protein Bax and inhibit the phosphorylation of PI3K/Akt by increasing the content of ROS, while LEO can promote the phosphorylation of PI3K/Akt and further promote the expression of eNOS, thus promoting the survival, proliferation, migration, and NO release of endothelial cells. At the same time, phosphorylated-Akt can also inhibit the expression of apoptotic proteins such as Bcl2 and Bax, thus inhibiting endothelial cell apoptosis induced by ROS. “←” indicates activation, and “⟝” indicates inhibition.</div>

Oxidative Medicine and Cellular Longevity

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Figure 9

Figure 9: Leonurine Ameliorates Oxidative Stress and Insufficient Angiogenesis by Regulating the PI3K/Akt-eNOS Signaling Pathway in H<sub>2</sub>O<sub>2</sub>-Induced HUVECs 

Figure 9 | Leonurine Ameliorates Oxidative Stress and Insufficient Angiogenesis by Regulating the PI3K/Akt-eNOS Signaling Pathway in H2O2-Induced HUVECs 