Abstract:
Anisodamine, an alkaloid isolated from the Chinese herb Anisodas tanguticus and later synthesized, has been used as an antishock drug in China for two decades. This study attempted to determine if anisodamine affects arachidonic acid metabolism in cultured cells. Results indicate that endotoxin-stimulated synthesis of cyclooxygenase products including prostacyclin (measured as 6-keto-PGF
1α), thromboxane A
2 (measured as TXB
2) and prostaglandin F
2α (PGF
2α) in mice peritoneal macrophages was dose-dependently inhibited by anisodamine at dosages of 0.1~0.5 mg/ml, Preincubation of macrophages with anisodamine (0.5 mg/ml) for 2 h significantly decreased subsequent endotoxin-stimulated 6-keto-PGF
1α and TXB
2 production, In
3H-arachidonic acid prelabelled bovine aorta endothelial cells, both the release of
3H-labelled compounds and-production of 6-keto-PGF
1α were inhibited by anisodamine. It is suggested that anisodamine directly inhibited endotoxin-stimulated prostaglandin synthesis by cells in culture and its site of action might be at the cyclooxygenase reaction or, more likely, at the process of deesterification of cellular lipids.