Abstract
Possible involvement of 5-hydroxytryptamine (5-HT), 5-HT receptors and prostaglandins in the acceleration of gastrointestinal transit by momordin Ic was investigated in mice. Accelerative effect of momordin Ic (25 mg/kg, p.o.) on gastrointestinal transit was attenuated by pretreatment with a bolus of dl-p-chlorophenylalanine methyl ester (an inhibitor of 5-HT synthesizing enzyme), but not repeated pretreatment with dl-p-chlorophenylalanine methyl ester. Furthermore, cyproheptadine (a nonselective 5-HT2 receptor antagonist), ritanserin (a 5-HT2A/2B/2C receptor antagonist) and clozapine (a 5-HT2A/2C receptor antagonist) also attenuated the effect of momordin Ic, but methiothepin (a 5-HT1 receptor antagonist), MDL 72222 (3-tropanyl-3,5-dichlorobenzoate) and metoclopramide (5-HT3 receptor antagonists), tropisetron (a 5-HT3/4 receptor antagonist), ketanserin and haloperidol (5-HT2A receptor antagonists) did not. These results suggested a possible involvement of endogenous 5-HT and 5-HT2B/2C over 5-HT2A receptors. Attenuation by pretreatment with indomethacin (an inhibitor of prostaglandins synthesis) suggested involvement of prostaglandins. It is postulated that momordin Ic accelerates gastrointestinal transit partially by stimulating synthesis of 5-HT to act through 5-HT2, possibly 5-HT2C and/or 5-HT2B receptors, which, in turn, increases synthesis of prostaglandins.
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