ABSTRACT
A new ajmaline-type alkaloid, 21-Ο-methylisoajmaline (1), together with twenty-one known compounds, a mixture of ß-sitosterol (2) and stigmasterol (3), reserpinine (4); tetrahydroalstonine (5), reserpine (6), venoterpine (7), yohimbine (8), 6'-O-(3,4,5-trimethoxybenzoyl)glomeratose A (9), isoajmaline (10), 3-epi-α-yohimbine (11), methyl 3,4,5-trimethoxy-trans-cinnamate (12), a mixture of ß-sitosterol 3-Ο-ß-D-glucopyranoside (13) and stigmasterol 3-Ο-ß-D- glucopyranoside (14), rescidine (15), 7-deoxyloganic acid (16), ajmaline (17), suaveoline (18), (+)-tetraphyllicine (19), loganic acid (20), 3-hydroxysarpagine (21), and sarpagine (22), were isolated from the roots of Rauvolla serpentina. Their structures were elucidated by spectroscopic data analysis and comparison with literature data. Compounds 11, 12 and 15 were for the first time identified from the genus Rauvolfla and 5, 7, 11, 12, 15, 18 and 22 were found from R. sepentina for the first time. Compound 11 showed moderate anticholinesterase activity with IC50 value of 15.58 µM, whereas 6 exhibited strong vasorelaxant activity with the EC50 value of 0.05 µM.
Subject(s)
Ajmaline/chemistry , Plant Extracts/chemistry , Rauwolfia/chemistry , Ajmaline/isolation & purification , Animals , Magnetic Resonance Spectroscopy , Male , Plant Extracts/isolation & purification , Plant Roots/chemistry , Rats , Rats, Sprague-Dawley , Vasodilator Agents/chemistry , Vasodilator Agents/isolation & purification , Vasodilator Agents/pharmacologyABSTRACT
Seven new ajmaline type alkaloids, alstiphyllanines I-O (1-7) were isolated from the leaves of Alstonia macrophylla together with six related alkaloids (8-13). Structures and stereochemistry of 1-7 were fully elucidated and characterized by 2D NMR analysis. A series of alstiphyllanines I-O (1-7) as well as the known ajmaline type alkaloids (8-13) showed that they relaxed phenylephrine (PE)-induced contractions against rat aortic ring. Among them, vincamedine (10) showed potent vasorelaxant activity, which may be mediated through inhibition of Ca(2+) influx through voltage-dependent Ca(2+) channels (VDCs) and/or receptor-operated Ca(2+) channels (ROCs) as well as partially mediated the NO release from endothelial cells. The presence of substituents at both N-1 and C-17 may be important to show vasorelaxation activity.