Table 2 |
||
| Summary of in vitro magnolol effect on cardiovascular system | ||
| 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 | [33,34] |
| 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] |
Ho and Hong Journal of Biomedical Science 2012 19:70 doi:10.1186/1423-0127-19-70