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The Effect of Ganodermic Acid S on Human Platelets

  • Chuen-Neu Wang
  • Jia-Chyuan Chen
  • Ming-Shi Shiao
  • Cheng-Teh Wang
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 281)

Summary

Incubation of gel-filtered human platelets in ganodermic acid S (lanosta-7,9(11), 24trien-3ß, 15α-diacetoxy-26-oic acid) showed that uptake of the agent by platelets was a simple diffusion process. The agent caused platelet aggregation at concentrations above 20μM. Above the threshold, the extent of cell aggregation was in a linear relationship to the agent concentration. Below the aggregation threshold, platelets showed neither the resynthesis of [32P] phosphatidylinositol 4,5-bisphosphate ([32P]PIP2) and [32P] phosphatidylinositol 4-phosphate ([32P]PIP) nor the accumulation of [32P] phosphatidic acid ([32P]PA). The results suggested that ganodermic acid S caused the activation of PIP2 hydrolysis. Scanning electron microscopy revealed that the morphology of platelets below the aggregation threshold appeared to be spiculate discoid shape. Above the threshold, the cells rounded up to spiculate irregular forms.

Keywords

Platelet Aggregation Phosphatidic Acid Agent Concentration Platelet Membrane Irregular Form 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1990

Authors and Affiliations

  • Chuen-Neu Wang
    • 1
  • Jia-Chyuan Chen
    • 1
  • Ming-Shi Shiao
    • 1
  • Cheng-Teh Wang
    • 1
  1. 1.Institute of Life ScienceNational Tsing Hua UniversityHsinchuTaiwan, ROC

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