Premium
Rosa laevigata Michx‐induced improvement of vascular dysfunction through PI3K/AKT‐mediated NO‐cGMP pathway in endothelial cells and 2K1C hypertensive rat
Author(s) -
Kim Hye Yoom,
Ahn You Mee,
Hong Mi Hyeon Hong,
Yoon Jung Joo,
Lee Yun Jung,
Kang Dae Gill,
Lee Ho Sub
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.691.4
Subject(s) - enos , nitric oxide , wortmannin , protein kinase b , pi3k/akt/mtor pathway , medicine , endothelium , pharmacology , phenylephrine , vasodilation , endothelial dysfunction , losartan , phosphorylation , endocrinology , chemistry , nitric oxide synthase , signal transduction , blood pressure , angiotensin ii , biochemistry
Rosa laevigata Michx has been used to treat chronic cough, arterial sclerosis, menstrual irregularities, and urinary incontinence. The purpose of the present study was to investigate the underlying cellular mechanisms of the nitric oxide (NO)‐mediated property of the aqueous extract of Rosa Laevigata Michaux (ARL). The roles of the NO signaling in the ARL‐induced effects were tested in HUVECs and aortic ring. HUVEC treated with ARL produced higher amount of NO compared to control. ARL increased in the expression and phosphorylation levels of eNOS and Akt in HUVECs, which were attenuated by L‐NAME, a NOS inhibitor, and wortmannin, a PI3K inhibitor. In addition, ARL‐induced dose‐dependent relaxation of phenylephrine‐precontracted aorta was abolished by removal of functional endothelium. Pretreatment with NO‐cGMP inhibited the ARL‐induced vasorelaxation. In addition, an upstream signaling molecule of eNOS, attenuated the ARL‐induced vasorelaxation. Incubation of endothelium‐intact aortic rings with ARL increased the production of cGMP, however, which were attenuated by L‐NAME and ODQ. Two‐kidney‐one‐clip (2K1C) hypertensive rats were established to investigate the hypotensive effect of ARL in renovascular hypertension. 2K1C rats were treated with ARL at dose of 100 mg/kg/day orally for 3 weeks. Consequently, ARL significantly lowered blood pressure, and ameliorates vascular relaxation in thoracic aorta. Taken together, the present study suggests that ARL ameliorates vascular dysfunction via the regulation of endothelium‐dependent activation of through the PI3K/Akt‐mediated NO‐cGMP signaling. Support or Funding Information This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .