Premium
Vasorelaxant effects of diarylheptanoids, acerogenin A and (−)‐centrolobol from the bark of Acer nikoense
Author(s) -
Iizuka Toru,
Nagumo Seiji,
Yotsumoto Hideomi,
Terabayashi Susumu,
Fukai Toshio,
Nagai Masahiro
Publication year - 2018
Publication title -
traditional and kampo medicine
Language(s) - English
Resource type - Journals
ISSN - 2053-4515
DOI - 10.1002/tkm2.1197
Subject(s) - chemistry , diarylheptanoids , bark (sound) , glibenclamide , vasoconstriction , aorta , ethyl acetate , aconitine , traditional medicine , pharmacology , chromatography , stereochemistry , anesthesia , medicine , endocrinology , physics , acoustics , diabetes mellitus
Aim The bark of Acer nikoense (Aceraceae) is used in Japanese folk medicine as a remedy for hepatic disorders and eye diseases. The aim of this study was to investigate the vasorelaxant effects of A. nikoense extracts and further clarify the active constituents and mechanisms of action. Methods Dried A. nikoense bark was extracted with methanol. The extract was further extracted with diethyl ether, ethyl acetate, and 1‐butanol, successively. The major constituents of the extracts were isolated using chromatography. Vasorelaxant effects of the extracts and isolated constituents were assessed using isolated rat aorta. The aorta was placed in a well‐oxygenated bath of modified Krebs–Henseleit solution and the mechanical tension measured isometrically. Results The extracts had a vasorelaxant effect on aorta precontracted with 3 × 10 −7 mol/L norepinephrine (NE). Isolated major constituents of A. nikoense bark, diarylheptanoids, such as acerogenin A (compound 1), B (compound 2), (−)‐centrolobol (compound 3), aceroside I (compound 5), B1 (compound 6), VII (compound 7) III (compound 8), and phenolic compound, (+)‐rhododendrol (compound 4) were examined. Compounds 1 and 3 had vasorelaxant effects on rat aorta with or without endothelium in the NE‐induced preparation. Furthermore, compounds 1 and 3 inhibited contraction induced by a high concentration (60 mmol/L) of K + and also had a moderate inhibitory effect on NE‐induced vasoconstriction in the presence of nicardipine. Conclusion The inhibition of NE‐induced vasoconstriction by compounds 1 and 3 may be attributed to factors such as endothelial independency by blocking of Ca 2+ influx via voltage‐dependent Ca 2+ channels and receptor‐operated Ca 2+ channels.