Oxymatrine Powder

Vascular endothelial cells have a variety of important physiological functions, such as regulating vascular tone, maintaining the balance between coagulation and fibrinolysis systems, regulating the aggregation of inflammatory cells, inhibiting platelet aggregation, etc. Endothelial cell damage and dysfunction are the initial steps in the formation of atherosclerotic lesions and are closely related to coronary heart disease and myocardial ischemia. Therefore, protecting vascular endothelial cells is an important strategy to prevent and treat cardiovascular diseases. Oxymatrine has protective effects. The role of various vascular endothelial cells.​​
1. Protect umbilical vein endothelial cells
In an in vitro experiment to study the anti-tumor angiogenesis of oxymatrine, human umbilical vein endothelial cells were used as a control. The results showed that the half inhibitory concentration (IC50) of oxymatrine in inhibiting the proliferation of human umbilical vein endothelial cells was 1555 mg/L. , can make cell nuclei deeply stained, cell volume smaller and irregular, extracellular villi reduced, most of them in an early apoptosis state, and can significantly inhibit the activity of succinate dehydrogenase in aerobic oxidation. Oxymatrine can concentration-dependently improve the low survival rate of human umbilical vein endothelial cells caused by hypoxia and reoxygenation, reduce the lactate dehydrogenase content in the culture medium, and increase the Bcl-2/Bax ratio and down-regulate caspases. -3 protein expression. Another study reported that oxymatrine did not affect the proliferation of human umbilical vein endothelial cells when the concentration was 1 and 3 μmol/L, but inhibited its proliferation when it was 10 and 30 μmol/L; 3 μmol/L can resist the effects of high glucose on human umbilical vein endothelial cells. Damage and decreased activity of endothelial cells; expression of A2B receptors and independent chemokine CCL5 receptors that can resist high glucose upregulation of adenosine, as well as phosphorylation of p38 and extracellular signal-regulated kinase 1/(2 ERK1/2) , indicating that the mechanism is that oxymatrine resists the damage of endothelial cells caused by high glucose by down-regulating the expression of A2B receptors.​​​​
2. Protect arterial and microvascular endothelial cells

Oxymatrine can promote endothelial cell proliferation at low concentrations, and its mechanism is related to inhibiting the secretion of vascular endothelial growth factors by tumor cells and downregulating the expression of growth factor receptors related to blood vessels. Studies have reported that intraperitoneal injection of oxymatrine 120 mg/kg for 10 consecutive days can reduce the protein expression of nuclear factor-κB (NF-κB), ERK1/2, p38MAPK and JNK in basilar artery endothelial cells in rats with subarachnoid hemorrhage. Gene expression of interleukin (LT)-1β, IL-6, and tumor necrosis factor-α (TNF-α). The relevant mechanism is related to down-regulating the expression of A2B receptors, blocking the MAPK/ERK/JNK signaling pathway, and inhibiting inflammatory responses. In addition, oxymatrine can inhibit endothelial-to-mesenchymal transition, protect vascular endothelial cells, and inhibit vascular remodeling by downregulating the expression of hypoxia-inducible factor-1α.