Gamma-aminobutyric acid-salt attenuated high cholesterol/high salt diet induced hypertension in miceGamma-aminobutyric acid-salt attenuated high cholesterol/high salt diet induced hypertension in mice
- Other Titles
- Gamma-aminobutyric acid-salt attenuated high cholesterol/high salt diet induced hypertension in mice
- Authors
- 손명주; 오세연; 이혜선; Junwon Choi; 이배진; Joung-Hyun Park; 박철현; 손국희; 변경희
- Issue Date
- Jan-2021
- Publisher
- 대한약리학회
- Keywords
- Blood pressure; Endothelial cells; Gamma-aminobutyric acid (GABA)-salt; Macrophage polarization; Smooth muscle cells
- Citation
- The Korean Journal of Physiology & Pharmacology, v.25, no.1, pp.27 - 38
- Journal Title
- The Korean Journal of Physiology & Pharmacology
- Volume
- 25
- Number
- 1
- Start Page
- 27
- End Page
- 38
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/79707
- DOI
- 10.4196/kjpp.2021.25.1.27
- ISSN
- 1226-4512
- Abstract
- Excessive salt intake induces hypertension, but several gamma-aminobutyric acid (GABA) supplements have been shown to reduce blood pressure. GABAsalt, a fermented salt by L. brevis BJ20 containing GABA was prepared through the post-fermentation with refined salt and the fermented GABA extract. We evaluated the effect of GABA-salt on hypertension in a high salt, high cholesterol diet induced mouse model. We analyzed type 1 macrophage (M1) polarization, the expression of M1 related cytokines, GABA receptor expression, endothelial cell (EC) dysfunction, vascular smooth muscle cell (VSMC) proliferation, and medial thicknesses in mice model. GABA-salt attenuated diet-induced blood pressure increases, M1 polarization, and TNF-α and inducible nitric oxide synthase (NOS) levels in mouse aortas, and in salt treated macrophages in vitro. Furthermore, GABA-salt induced higher GABAB receptor and endothelial NOS (eNOS) and eNOS phosphorylation levels than those observed in salt treated ECs. In addition, GABA-salt attenuated EC dysfunction by decreasing the levels of adhesion molecules (E-selectin, Intercellular Adhesion Molecule- 1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1]) and of von Willebrand Factor and reduced EC death. GABA-salt also reduced diet-induced reductions in the levels of eNOS, phosphorylated eNOS, VSMC proliferation and medial thickening in mouse aortic tissues, and attenuated Endothelin-1 levels in salt treated VSMCs. In summary, GABA-salt reduced high salt, high cholesterol diet induced hypertension in our mouse model by reducing M1 polarization, EC dysfunction, and VSMC proliferation.
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