Table 2 Summary of in vitro magnolol effect on cardiovascular system
From: Cardiovascular protection of magnolol: cell-type specificity and dose-related effects
Concentration | Effect | Reference |
|---|---|---|
Low (≦1 μM) to Moderate | ||
0.1‒10 μM | Diminish PMA‒induced neutrophil activation and reduce neutrophil adhesion ability | [44] |
Moderate (1–100 μM) | ||
5‒10 μM | Inhibited TNFα‒induced VACM‒1 expression in aortic endothelial cells | [37] |
10 μM | Inhibit proliferation of cardiac fibroblasts | [23] |
16.8 μM | Inhibit LPS‒induced macrophage activation | [35] |
5‒20 μM | Induce intrinsic apoptosis in vascular smooth muscle cells | [25] |
5‒20 μM | Inhibit TNFα‒induced vascular smooth muscle cell proliferation | [27] |
>20 μM | Downregulate IL‒6‒induced ICAM‒1 expression in endothelial cells and suppress monocyte adhesion to endothelial cells | [41] |
2.5‒20 μM | Inhibit copper‒induced ox‒LDL triggered endothelial cell apoptosis | |
24.2 μM | Inhibit neutrophil aggregation | [38] |
3‒30 μM | Inhibit collagen‒induced platelet serotonin release | [43] |
5‒50 μM | Suppress fMLP‒activated neutrophil migration | [20] |
30‒90 μM | induce cytosolic‒free Ca2+ elevation in neutrophil | [36] |
Moderate to High (≧100 μM) | ||
200 μM | Reduce serum‒induced vascular smooth muscle cell proliferation | [26] |
40‒400 μM | block norepinephrine‒ or high K+−induced contraction of aorta | [30] |
60‒150 μM | Inhibit biosynthesis of platelet‒activating factor from PMNs | [44] |