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Dihydromyricetin increases endothelial nitric oxide production and inhibits atherosclerosis through microRNA-21 in apolipoprotein E-deficient mice.

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收录情况： ◇ SCIE

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机构： [1]Department of Pharmacy, Institute of Clinical Pharmacy, Second Xiangya Hospital, Central South University, Changsha, China. [2]Department of Cardiovascular Surgery, Second Xiangya Hospital, Central South University, Changsha, China. [3]Department of Pharmacy, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China. [4]Department of Pharmacy, Affiliated Changsha Hospital of Hunan Normal University, Changsha, China. [5]Department of Geriatrics, National Key Clinic Specialty, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China. [6]Department of Cardiology, Third Xiangya Hospital, Central South University, Changsha, China. [7]Department of Cardiology, Vascular Center, Guangdong Cardiovascular Institute, Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China. [8]Department of General Surgey, Second Xiangya Hospital, Central South University, Changsha, China. [9]School of Pharmacy, Hunan University of Chinese Medicine, Changsha, China. [10]Department of Pharmacy, The Third Hospital of Changsha, Changsha, China. [11]The Second Affiliated Hospital of University of South China, Hengyang, China. [12]New Drugs Innovation and Development Institute, Department of Pharmacy, College of Medicine, Wuhan University of Science and Technology, Wuhan, China. [13]Department of Clinical Pharmacy and Pharmacology, Jining First People's Hospital, Jining Medical University, Jining, China.

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关键词： atherosclerosis dihydromyricetin endothelial cell microRNA nitric oxide

摘要：

Natural products were extracted from traditional Chinese herbal emerging as potential therapeutic drugs for treating cardiovascular diseases. This study examines the role and underlying mechanism of dihydromyricetin (DMY), a natural compound extracted from Ampelopsis grossedentata, in atherosclerosis. DMY treatment significantly inhibits atherosclerotic lesion formation, proinflammatory gene expression and the influx of lesional macrophages and CD4-positive T cells in the vessel wall and hepatic inflammation, whereas increases nitric oxide (NO) production and improves lipid metabolism in apolipoprotein E-deficient (Apoe-/- ) mice. Yet, those protective effects are abrogated by using NOS inhibitor L-NAME in Apoe-/- mice received DMY. Mechanistically, DMY decreases microRNA-21 (miR-21) and increases its target gene dimethylarginine dimethylaminohydrolase-1 (DDAH1) expression, an effect that reduces asymmetric aimethlarginine (ADMA) levels, and increases endothelial NO synthase (eNOS) phosphorylation and NO production in cultured HUVECs, vascular endothelium of atherosclerotic lesions and liver. In contrast, systemic delivery of miR-21 in Apoe-/- mice or miR-21 overexpression in cultured HUVECs abrogates those DMY-mediated protective effects. These data demonstrate that endothelial miR-21-inhibited DDAH1-ADMA-eNOS-NO pathway promotes the pathogenesis of atherosclerosis which can be rescued by DMY. Thus, DMY may represent a potential therapeutic adjuvant in atherosclerosis management. © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.

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出版当年[2019]版：

大类 | 2 区医学

小类 | 2 区医学：研究与实验 3 区细胞生物学

最新[2025]版：

大类 | 3 区医学

小类 | 3 区细胞生物学 3 区医学：研究与实验

JCR分区：

出版当年[2018]版：

Q1 MEDICINE, RESEARCH & EXPERIMENTAL Q2 CELL BIOLOGY

最新[2023]版：

Q2 CELL BIOLOGY Q2 MEDICINE, RESEARCH & EXPERIMENTAL

影响因子： 4.3 最新[2023版] 5.1 最新五年平均 4.658 出版当年[2018版] 4.408 出版当年五年平均 4.302 出版前一年[2017版] 4.486 出版后一年[2019版]

第一作者：

第一作者机构： [1]Department of Pharmacy, Institute of Clinical Pharmacy, Second Xiangya Hospital, Central South University, Changsha, China. [2]Department of Cardiovascular Surgery, Second Xiangya Hospital, Central South University, Changsha, China.

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通讯作者：

通讯机构： [1]Department of Pharmacy, Institute of Clinical Pharmacy, Second Xiangya Hospital, Central South University, Changsha, China. [*1]Department of Pharmacy, Institute of Clinic Pharmacy, Second Xiangya Hospital, Central South University, 139 Renmin Road Central, Changsha, Hunan 410011, China

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Dihydromyricetin increases endothelial nitric oxide production and inhibits atherosclerosis through microRNA-21 in apolipoprotein E-deficient mice.

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