Relaxin Ameliorates Renal Fibrosis and Expression of Endothelial Cell Transition Markers in Rats of Isoproterenol-Induced Heart Failure
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- Zheng Gaoshu
- Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University
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- Cai Jiejie
- Department of Intensive Care Unit, The First Affiliated Hospital of Wenzhou Medical University
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- Chen Xingxing
- Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University
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- Chen Lingzhi
- Department of Clinical Laboratory, Wenzhou Central Hospital
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- Ge Wenhua
- Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University
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- Zhou Xi
- Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University
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- Zhou Hao
- Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University
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説明
<p>There may be cardio–renal interactions in rats of isoproterenol-induced heart failure, which may be associated with renal fibrosis and endothelial-to-mesenchymal transition (EndMT). Since its discovery, relaxin (RLX) which was regarded as a reproductive hormone for a long time, is recently considered an effective antifibrotic hormone in cardiac and renal fibrosis. We studied whether RLX diminished renal fibrosis in rats of isoproterenol (Iso)-induced heart failure and investigated the mechanism. Fifty male Sprague–Dawley rats were separated into five groups for treatment: control; Iso subcutaneously injection to induce heart failure, which led to renal fibrosis; RLX subcutaneously injection at low, medium and high dose (0.2, 2, 20 µg·kg−1·d−1 for 21 d). Indices of cardiac function and organ fibrosis were examined. Expression and changes in levels of collagen, cluster of differentiation 31 (CD31), α-smooth muscle actin (SMA), and transforming growth factor β (TGF-β) were measured in renal tissues. In rats with heart failure induced by Iso, treatment with RLX significantly ameliorated cardiac function and inhibited cardiac and renal fibrosis. RLX decreased renal collagen types I and III deposition, increased CD31 expression, and decreased the expression of α-SMA and TGF-β, thereby possibly indicating inhibited renal EndMT in kidneys. Iso-induced heart and renal fibrosis was inhibited even greater with high-dose RLX, so the antifibrotic effect of RLX may be dose-related. In conclusion, RLX may ameliorate renal fibrosis in rats of Iso-induced heart failure, and it is infered that prevention of the EndMT may be one of the possible potential signaling pathways.</p>
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 40 (7), 960-966, 2017
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001204631269376
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- NII論文ID
- 130006846415
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 028313084
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- PubMed
- 28674260
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可