Royal jelly enhances mouse intestinal motility via acetylcholine receptor activation

[Speaker] Shino Miyauchi-Wakuda:1
[Co-author] Hikari Kozuke:1, Mayu Kimoto:1, Satomi Kagota:1, Yoshihiko Ito:2, Kana Maruyama:1, Hirokazu Wakuda:3, Shizuo Yamada:2, Kazumasa Shinozuka:1
1:Department of Pharmacology, School of Pharmacy and Pharmaceutical Sciences, Mukogawa Women's University, Japan, 2:Center for Pharma-Food Research, Division of Pharmaceutical Sciences, Graduate School of Integrative Pharmaceutical and Nutritional Sciences, University of Shizuoka, Japan, 3:Department of Clinical Pharmacology and Therapeutics, Faculty of Medicine, Oita University, Japan

Constipation, a common problem in daily life, is caused by functional and structural abnormalities. Empirically, it is known that royal jelly (RJ) can be used to relieve autonomic dysfunction or constipation. It has been reported that RJ contains acetylcholine (ACh) and induces contractions, which are antagonized by treatment with a muscarinic receptor blocker, atropine (Atr), in the ileum of guinea pigs in in vitro experiments. However, insufficient data exist to elucidate the mechanism responsible for the improvement of constipation. In this study, the mechanisms of RJ-induced intestinal contraction were investigated by using isolated mouse ileum.
 The ileum was isolated from ICR mice; 10-mm-wide segments were mounted in an organ bath chamber filled with Krebs-Henseleit solution and bubbled with 95% O2/5% CO2 gas. ACh, RJ, and nicotine were cumulatively added to the bath. The effects of pretreatment with Atr, physostigmine (an ACh esterase (AChE) inhibitor), and NG-nitro-L-arginine methyl ester (L-NAME; a NOS inhibitor) were determined based on ACh- and RJ-induced contractions. Furthermore, ACh and RJ were incubated with recombinant mouse AChE for 5 min and then applied to the ileal segments.
 ACh and RJ induced contractions in a dose-dependent manner; these contractions were reduced by treatment with Atr and increased by treatment with physostigmine. The incubation of ACh or RJ with AChE did not cause contractions. Nicotine also induced contractions in a dose-dependent manner, which were increased by pretreatment with L-NAME. However, L-NAME did not affect RJ-induced contractions.
 These results suggest that ACh is an active component of RJ and causes ileal contractions via the muscarinic receptors in smooth muscle cells. RJ may not stimulate nitrergic neurons via nicotinic receptors. Although further studies are necessary in this regard, RJ may be a dietary supplement or an alternative medicine for constipation through the enhancement of motility.
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