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대메뉴안내: 농수식품
농림성과 수산성과 식품성과 인터뷰
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최재일 (J Choi) 저자 이메일 보기
계명대학교 의과대학
조회 351  인쇄하기 주소복사 트위터 공유 페이스북 공유 
Role of the histone deacetylase inhibitor valproic acid in high-fat diet-induced hypertension via inhibition of HDAC1/angiotensin II axis

J Choi1, S Park1, T K Kwon2, S-I Sohn3, K M Park4 and J I Kim1,*

1
Department of molecular Medicine and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea
2Department of Immunology and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea
3Department of Neurology and Medical Research Center, Keimyung University School of Medicine, Daegu, Republic of Korea
4Department of Anatomy and BK21 plus, Kyungpook National University School of Medicine, Daegu, Republic of Korea

*Correspondence: Professor JI Kim, Department of Molecular Medicine and Medical Research Center, Keimyung University School of Medicine, 1095 Dalgubeol-Daero, Dalseo-Gu, Daegu 42601, Republic of Korea.

Abstract
BACKGROUND: Obesity is known as an epidemic worldwide because of consumption of westernized high-fat diets and one of the major risk factors of hypertension. Histone deacetylases (HDACs) control gene expression by regulating histone/non-histone protein deacetylation. HDAC inhibitors exert anti-cancer and anti-inflammatory effects and play a protective role in cardiovascular diseases. In the present study, we tested the effect of an FDA-approved pan-HDAC inhibitor valproic acid (VPA) on high-fat diet (HFD)-induced hypertension in mice. Further, we examined the mechanism of VPA-induced prevention of hypertension.

METHODS: Nine-week-old male C57BL/6 mice were fed either a normal diet (ND) or HFD. When the HFD group reached a pre-hypertensive phase (130-140 mm Hg systolic blood pressure), VPA was administered for 6 days (300mg·kg-1·day-1). Body weights and blood pressure (BP), expression of renin-angiotensin system (RAS) components and HDAC1 were determined. The direct role of HDAC1 in the expression of RAS components was investigated using gene silencing.

RESULTS: HFD accelerated the increase in body weight from 22.4±1.3 to 31.9±3.0 compared to in the ND group from 22.7±0.9 to 26.0±1.7 (P=0.0134 ND vs HFD), systolic BP from 118.5±5.7 to 145.0±3.0 (P<0.001), and diastolic BP from 91.0±13.6 to 121.0±5.0 (P=0.006); BP was not altered in the ND group. HFD increased RAS components and HDAC1 in the kidneys as well as leptin in the plasma. VPA administration prevented the progression of hypertension and inhibited the increase in expression of HDAC1 and RAS components. VPA did not affect plasma leptin level. Knockdown of HDAC1 in MDCK cells decreased the expression of angiotensinogen and type1 angiotensin II receptor.

CONCLUSIONS: VPA prevented HFD-induced hypertension by downregulating angiotensin II and its receptor via inhibition of HDAC1, offering a novel therapeutic option for HFD-induced hypertension.

논문정보
- 형식: Research article
- 게재일: 2017년 07월 (BRIC 등록일 2017-08-03)
- 연구진: 국내연구진 태극기
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