METHODS AND RESULTS:
Clausine D inhibited concentration-dependently the aggregation and release reaction of washed rabbit platelets induced by arachidonic acid and collagen, without affecting those induced by U46619, PAF and thrombin. The IC50 values of Clausine D on arachidonic acid- and collagen-induced platelet aggregation were calculated to be 9.0 +/- 1.1 and 58.9 +/- 0.9 microM, respectively. Thromboxane B2 and prostaglandin D2 formation in platelets caused by arachidonic acid were also suppressed. Clausine D inhibited increased intracellular concentration of calcium in platelets caused by arachidonic acid and collagen, and also abolished the generation of inositol monophosphate caused by arachidonic acid, but not that by collagen, U46619, PAF and thrombin. In human citrated platelet-rich plasma, Clausine D inhibited the secondary phase, but not the primary phase, of aggregation induced by epinephrine and ADP.
CONCLUSIONS:
These results indicate that the antiplatelet effect of Clausine D is due to inhibition of the formation of thromboxane A2. |
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)
