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千层纸素A改善大鼠慢性心力衰竭的作用及其分子机制

王晶晶, 田晨光, 张金盈, 张继佳, 吴照科

王晶晶, 田晨光, 张金盈, 张继佳, 吴照科. 千层纸素A改善大鼠慢性心力衰竭的作用及其分子机制[J]. 中国药科大学学报, 2018, 49(6): 731-738. DOI: 10.11665/j.issn.1000-5048.20180615
引用本文: 王晶晶, 田晨光, 张金盈, 张继佳, 吴照科. 千层纸素A改善大鼠慢性心力衰竭的作用及其分子机制[J]. 中国药科大学学报, 2018, 49(6): 731-738. DOI: 10.11665/j.issn.1000-5048.20180615
WANG Jingjing, TIAN Chenguang, ZHANG Jinying, ZHANG Jijia, WU Zhaoke. Oroxylin A ameliorates isoproterenol-induced heart failure model in rats through promoting myocardial autophagy[J]. Journal of China Pharmaceutical University, 2018, 49(6): 731-738. DOI: 10.11665/j.issn.1000-5048.20180615
Citation: WANG Jingjing, TIAN Chenguang, ZHANG Jinying, ZHANG Jijia, WU Zhaoke. Oroxylin A ameliorates isoproterenol-induced heart failure model in rats through promoting myocardial autophagy[J]. Journal of China Pharmaceutical University, 2018, 49(6): 731-738. DOI: 10.11665/j.issn.1000-5048.20180615

千层纸素A改善大鼠慢性心力衰竭的作用及其分子机制

基金项目: 国家自然科学基金资助项目(No.81570274)

Oroxylin A ameliorates isoproterenol-induced heart failure model in rats through promoting myocardial autophagy

  • 摘要: 探讨千层纸素A(oroxylin A,OA)对异丙肾上腺素诱导的大鼠心力衰竭的保护作用及其分子机制。与模型组相比,OA给药组[25、50、100 mg/(kg·d),每组8只大鼠,灌胃给药8周]可剂量依赖地改善大鼠心力衰竭的症状,血流动力学参数和心脏射血分数有较大改善,心脏功能指数明显恢复,心脏彩超及苏木精-伊红染色、Masson染色提示心脏损伤程度明显减轻,多种神经内分泌因子如去甲肾上腺素、醛固酮、脑钠肽等在OA给药组均显著下调。进一步利用大鼠原代心肌细胞发现,OA可通过抑制AKT1-RPS6KB1信号通路促进心肌细胞自噬。实验结果表明,OA可通过促进心肌细胞的自噬来改善异丙肾上腺素所诱导的大鼠心力衰竭。
    Abstract: The protective effect and mechanism of Oroxylin A, a naturally occurring compound in Scutellaria baicalensis Georgi, was investigated in this study. Isoproterenol administration to rats triggered classic cardiac failure, as demonstrated by objective parameters of cardiac dysfunction. Intragastric administration of oroxylin A at the dose of 25, 50 and 100 mg/(kg·d)significantly improved deranged cardiac parameters in the isoproterenol-induced heart failure model in a dose-dependent manner. At the same time, oroxylin A markedly ameliorated cardiac histological changes and down-regulated serum levels of various neuroendocrine factors including norepinephrine, aldosterone, brain natriuretic peptide, endothelin 1, angiotensin II and so on. Mechanistically, augmenting autophagy of myocardial cells via the inhibition of AKT1-RPS6KB1 signaling contributed to the improvement of isoproterenol-induced rat heart failure by oroxylin A. Taken together, these results suggest that oroxylin A ameliorates heart failure through promoting autophagy in myocardial cells.
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出版历程
  • 刊出日期:  2018-12-24

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