Gamma-aminobutyric acid-salt attenuated high cholesterol/high salt diet induced hypertension in mice
10.4196/kjpp.2021.25.1.27
- Author:
Myeongjoo SON
1
;
Seyeon OH
;
Hye Sun LEE
;
Junwon CHOI
;
Bae-Jin LEE
;
Joung-Hyun PARK
;
Chul Hyun PARK
;
Kuk Hui SON
;
Kyunghee BYUN
Author Information
1. Department of Anatomy and Cell Biology, Gachon University College of Medicine, Korea
- Publication Type:Original Article
- From:The Korean Journal of Physiology and Pharmacology
2021;25(1):27-38
- CountryRepublic of Korea
- Language:English
-
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.
