|
| Name | Mechanism | Model | References |
|
TS IIA
AS IV | Inhibit the translocation of NF-κB to the nucleus and the expression of TLR4. Enhance vascular stability through PI3K/Akt and TLR4/NF-κB signals, reduce inflammation and MMP-9 expression, and inhibit unstable plaques. | ApoE−/– mouse | [48] |
| Breviscapine | Reduce the levels of inflammatory factors of VCAM-1, ICAM-1, IL-6, and TNF-α; reduce the blood lipid levels of SD rats; and reduce cell apoptosis.
PI3K/Akt signaling pathway activates Nrf2 to protect cells. | SD rat | [55,61] |
| Gypenoside | Activate the PI3K/Akt/Bad signaling pathway, regulate the expression of aortic cell apoptosis-related proteins, and downregulate mitochondrial deletion and fusion proteins and mitochondrial energy-related proteins. | ApoE−/– mouse | [59] |
| Gypenoside XVII | Activation of ERα-mediated PI3K/Akt pathway, Nrf2/HO-1 up-regulation, and the level of antioxidant enzymes; reduce ox-LDL-induced oxidative damage; and inhibit ox-LDL-mediated HUVEC apoptosis. | HUVECs ApoE−/– mouse | [60] |
| Salidroside | Improve endothelial function related to increased eNOS activation, activate AMPK, and improve endothelial function by activating mitochondrial-related AMPK/PI3K/Akt/eNOS pathway. | HUVECs ApoE−/– mouse | [16] |
| Iso | Activate PI3K/Akt signal, upregulate THP-1-derived macrophages HO-1, prevent ox-LDL-induced apoptosis, and inhibit lipid deposition in ox-LDL-induced macrophage apoptosis. | ApoE–/– mouse | [6] |
| Quercetin | High fructose activates ROS and inactivates the PI3K/Akt signaling pathway, causing apoptosis and inflammation through the Bcl-2/caspase-3 and IKKa/NF-kB signaling pathways, respectively. Quercetin improves and inhibits the progression of ROS AS through PI3K/Akt. | C57BL/6 induced by high fructose | [51] |
| Emodin | Regulate blood lipids, inhibit the mTOR signal pathway and PI3K/Akt signal activity, stimulate the body to increase autophagy, and increase the metabolism of glycolipids. | ApoE−/– mouse | [53] |
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