文献

J-GLOBAL ID：202202258633540353   整理番号：22A1039935

T1AMはRIPK1/RIPK3経路を介してH9C2心筋細胞の低酸素/再酸素化誘発ネクロップーシスを減弱する【JST・京大機械翻訳】

T1AM Attenuates the Hypoxia/Reoxygenation-Induced Necroptosis of H9C2 Cardiomyocytes via RIPK1/RIPK3 Pathway

著者 (16件)： Wei Bo (Department of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Wei Bo (Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Wei Bo (Department of Electrocardiogram, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Zhao Hanbing (Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Hu Bailong (Department of Anesthesiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Dai Lujun (Department of Pathology, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Zhang Guoning (Department of Cardiovascular Medicine, The Hospital of Qingzhen, Guiyang, Guizhou Province 550004, China) ,  Mo Lili (Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Huang Niwen (Department of Respiratory Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Zou Changchao (Department of Cardiovascular Medicine, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou Province 550004, China) ,  Zhang Bei (Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Zhou Haiyan (Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Li Wei (Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Liu Xingde (Department of Basic Medicine, Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Liu Xingde (Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou Province 550004, China) ,  Liu Xingde (Department of Cardiovascular Medicine, The Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine, Guiyang, Guizhou Province 550004, China)
資料名： BioMed Research International (Web)  (BioMed Research International (Web))
巻： 2022  ページ： Null  発行年： 2022年 
JST資料番号： U7008A  ISSN： 2314-6133  資料種別： 逐次刊行物 (A)
記事区分： 原著論文  発行国： イギリス (GBR)  言語： 英語 (EN)

抄録/ポイント： 目的.低酸素/再酸素化(H/R-)誘発H9C2損傷の細胞アポトーシスとプログラム壊死における3-ヨードチロンアミン(T1AM)の詳細な機構を研究する。心筋細胞H9C2細胞を心筋細胞H/Rモデルの確立のためにin vitroで培養した。細胞を4つの群にランダムに分けた:対照群,H/R群,T1AM前処置およびH/R(6μmT1AM+H/R)群。CCK8による心筋細胞阻害率の検出と乳酸デヒドロゲナーゼ(LDH)活性の検出により心筋損傷の程度を測定した。細胞アポトーシスをTUNELアッセイとフローサイトメトリー分析により評価した。ウェスタンブロット法とqRT-PCRによって,RIPK1,RIPK3,およびCAMKIIの蛋白質レベルとmRNAレベルを検出した。【結果】対照群と比較して,細胞抑制率はH/R群で劇的に上昇した。心筋細胞のLDH放出は有意に増加した。RIPK1,RIPK3およびCAMKIIの蛋白質およびmRNA発現は有意に増加した。H/R群と比較して,T1AM+H/R群のRIPK1,RIPK3,およびCAMKIIの細胞阻害率,LDH放出,心筋細胞壊死率,および蛋白質およびmRNAレベルは有意に減少した。【結語】T1AMによる前処理は心筋細胞のH/R損傷を軽減し,心筋細胞の壊死を阻害し,それはRIPK1/RIPK3経路の活性化で保護機能を発揮する可能性がある。Copyright 2022 Bo Wei et al. Translated from English into Japanese by JST.【JST・京大機械翻訳】

シソーラス用語： mRNA ,  壊死 ,  タンパク質 ,  乳酸デヒドロゲナーゼ ,  フローサイトメトリー ,  遺伝子発現 ,  心筋疾患 ,  in vitro実験 ,  アポトーシス ,  ウェスタンブロット法 ,  TUNEL法 ,  *心筋細胞
準シソーラス用語： mRNA発現 ,  *RIPK3 ,  qRT-PCR法 ,  *RIPK1 , 【Automatic Indexing@JST】

分類 (1件)： 細胞生理一般  (EF02010S)

引用文献 (22件)：

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タイトルに関連する用語 (8件)： RIPK1 ,  RIPK3 ,  経路 ,  心筋細胞 ,  低酸素 ,  再酸素化 ,  誘発 ,  減弱