Table 3.

Effect of TCM on endothelial dysfunction in DM.

TCM name	Active component	Mechanism of action	Main findings	References
Tanshinone IIA	Lipophilic diterpenoids	Inhibits NADPH oxidase, reduces oxidative stress, enhances eNOS expression, and promotes NO production	Improves endothelial-dependent relaxation and endothelial function	(144, 145)
Berberine	Isoquinoline alkaloid	Inhibits NF-κB activity, reduces inflammatory responses	Protects against vascular damage and anti-atherosclerosis	(150–156)
Resveratrol	Polyphenol compound	Activates SIRT1, upregulates Nrf2, and reduces ROS production	Prevents endothelial cell aging, reduces oxidative stress	(139, 141, 142)
Puerarin	Isoflavone glycoside	Regulates NF-κB, inhibits NOX2 and NOX4-mediated oxidative stress	Protects the aorta of diabetic rats by reducing cell adhesion molecule expression	(146)
Curcumin	Polyphenolic compound	Blocks AMPL/p38 MAPK pathway	Protects endothelial cells from oxidative stress in diabetic rats	(138–140)
Matrine alkaloids	Sophora alkaloids	Activates MKK3/p38 MAPK/Nrf2 signaling pathway, reduces AGEs-induced apoptosis	Prevents apoptosis of diabetic endothelial cells	(143)
Astragaloside IV	Triterpene saponin	Modulates glucose/lipid metabolism, inhibits TGF-β1/Smad signaling, reduces oxidative stress	Protects aortic endothelial cells and inhibits NF-κB activation	(148, 149)
Danshensu + Paeonol	Phenolic acids	Inhibits p38 MAPK signaling, enhances BKCa protein expression in vascular smooth muscle cells	Reduces vascular endothelial cell apoptosis in diabetic conditions	(144, 145)
Quercetin	Flavonoids compounds	Increases the expression of ABCA1, ABCG1 and CYP7A1, promoted cholesterol efflux from macrophages, down-regulated the expression of p53, p21, p16 and ERK, enhanced autophagy to anti-apoptosis, and inhibited MCP-1 and inflammatory cytokines	Reduces ROS and releases NOS to protect endothelial cells	(157–162)