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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제25권 제1호
- 발행연도
- 2021.1
- 수록면
- 27 - 38 (12page)
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초록· 키워드
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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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참고문헌 (59)
참고문헌 신청
World Health Organization (WHO) / 2009 / Global health risks: mortality and burden of disease attributable to selected major risks / World Health Organization
Liu G / 2014 / High sodium augments angiotensin II-induced vascular smooth muscle cell proliferation through the ERK 1/2-dependent pathway / Hypertens Res 37:13~18
Manning RD Jr / 2001 / Role of abnormal nitric oxide systems in salt-sensitive hypertension / Am J Hypertens 1(6 Pt 2):68S~73S
Chiong M / 2013 / Influence of glucose metabolism on vascular smooth muscle cell proliferation / Vasa 42:8~16
Liu Y / 1999 / Loss of endothelium and receptormediated dilation in pial arterioles of rats fed a short-term high salt diet / Hypertension 33:686~688
Liu G / 2014 / High sodium augments angiotensin II-induced vascular smooth muscle cell proliferation through the ERK 1/2-dependent pathway / Hypertens Res 37:13~18
Manning RD Jr / 2001 / Role of abnormal nitric oxide systems in salt-sensitive hypertension / Am J Hypertens 1(6 Pt 2):68S~73S
Chiong M / 2013 / Influence of glucose metabolism on vascular smooth muscle cell proliferation / Vasa 42:8~16
Liu Y / 1999 / Loss of endothelium and receptormediated dilation in pial arterioles of rats fed a short-term high salt diet / Hypertension 33:686~688
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