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J Physiol Pharmacol. 2017 Apr;68(2):215-221.

Mantidis ootheca induces vascular relaxation through PI3K/AKT-mediated nitric oxide-cyclic GMP-protein kinase G signaling in endothelial cells.

Kim HY1,2, Lee YJ1,2, Han BH1,2, Yoon JJ1,2, Ahn YM1,2, Hong MH2,3, Tan R1,2, Kang DG4,2,3, Lee HS1,5.

Author information

1
College of Oriental Medicine and Professional Graduate School of Oriental Medicine, Wonkwang University, Shinyong-dong, Iksan, Korea.
2
Hanbang Body-fluid Research Center, Wonkwang University, Shinyong-dong, Ikson, Korea.
3
Department of Food Industry Convergence, Wonkwang University, Shinyong-dong, Iksan, Korea.
4
College of Oriental Medicine and Professional Graduate School of Oriental Medicine, Wonkwang University, Shinyong-dong, Iksan, Korea. dgkang@wku.ac.kr.
5
Hanbang Body-fluid Research Center, Wonkwang University, Shinyong-dong, Ikson, Korea. host@wku.ac.kr.

Abstract

Mantidis ootheca (Sang Piao Xiao) is well known mantis eggs in a foamy pouch. The purpose of the present study was to investigate the underlying cellular mechanisms of the nitric oxide (NO)-releasing property of the aqueous extract of Mantidis ootheca (AMO) in rat aorta and vascular endothelial cells. AMO was examined for its vascular relaxant effect in isolated phenylephrine-precontracted rat thoracic aortic rings. The roles of the nitric oxide (NO) signaling in the AMO-induced effects were tested in human umbilical vein endothelial cells (HUVECs). HUVEC treated with AMO produced higher amount of NO compared to control. However, AMO-induced increases in NO production were blocked by pretreatment with NG-nitro-L-arginine methylester (L-NAME) or wortmannin. AMO increased in phosphorylation levels of endothelial nitric oxide synthase (eNOS) and Akt in HUVECs, which were attenuated by a NOS and Akt inhibitors. In aortic ring, AMO-induced dose-dependent relaxation of phenylephrine-precontracted aorta was abolished by removal of functional endothelium. Pretreatment with L-NAME, 1H-[1,2,4]-oxadiazolo-[4,3-alpha]-quinoxalin-1-one (ODQ), and KT5823 inhibited the AMO-induced vasorelaxation. Similarly, wortmannin and LY-294002, an inhibitors of the phosphatidylinositol 3-kinase (PI3K), an upstream signaling molecule of eNOS, attenuated the AMO-induced vasorelaxation. Moreover, AMO-induced increases in cGMP production were blocked by pretreatment with L-NAME or ODQ. The vasorelaxant effect of AMO was attenuated by tetraethylammonium, 4-aminopyridine, and glibenclamide. We conclude that AMO relaxed vascular smooth muscle via endothelium-dependent activation of PI3K/Akt-mediated NO-cGMP-PKG signaling pathway and possible involvement of K+ channel.

PMID:
28614771
[Indexed for MEDLINE]
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