SOME PHARMACOLOGICAL STUDIES OF ARDISIACRISPIN B, AN UTERO-CONTRACTING SAPONIN, ISOLATED FROM ARDISIA CRISPA

C. JANSAKUL

ABSTRACT: The present study aimed to characterize the pharmacologic action of the ardisiacrispin B. Studies were performed on in vitro preparations of uterine smooth muscle, small intestine and thoracic aorta (vascular smooth muscle) obtained from female rats in estrus. Dose- response curves (DR-curve) to ardisiacrispin B, prostaglandin E₂ derivative (Nalador), oxytocin and acetylcholine chloride were obtained. The possible involvement of prostaglandin synthesis in the utero-contracting activity of ardisiacrispin B was explored by investigation of the DR-curve to ardisiacrispin B in the presence of 10^-6 M indomethacin, a cyclo-oxygenase inhibitor. The local effects of the compound on uterine contractility and cervix softening were also studied in situ and in vitro respectively.
Ardisiacrispin B caused dose-dependent contraction of uterine smooth muscle, small intestine and thoracic aortae in a similar pattern to prostaglandin E₂ derivative. Oxytocin also caused uterine strip contraction but had no effect on small intestine. Acetylcholine caused uterine and small intestine contraction in a different manner from that obtained with ardisiacrispin B. However, the presence of indomethacin did not alter the DR-curve to ardisiacrispin B of uterine smooth muscle. In the in situ experiments, intra-uterine injections of ardisiacrispin B caused uterine contraction in a dose-dependent manner similar to those obtained from prostaglandin E₂ with no changes in mean arterial blood pressure, except that the highest concentration of ardisiacrispin B (6 mg/ml). caused lowering blood pressure in some animals. There were no signs of cervix softening after intra-uterine administration of either ardisiacrispin B or prostaglandin E₂, when compared with intra-uterine injections of saline. These results suggest that ardisiacrispin B may exert a prostaglandin E₂-like effect which may act at the prostaglandin E₂-receptor but not by stimulation or enhancement of prostaglandin synthesis.

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Department of Biology, Faculty of Science, Prince of Songkla University, Hat- Yai, Thailand, Telefax 66 074 212917

Received November 11, 1994