文章摘要
熊去氧胆酸对阿霉素诱导的H9c2心肌细胞的影响及机制研究*
Effects of Ursodeoxycholic Acid on doxorubicin-induced injury in H9c2 cardiomyocytes and Its Mechanism*
投稿时间:2020-07-28  修订日期:2020-07-28
DOI:
中文关键词: 熊去氧胆酸  阿霉素  心肌保护  炎症  凋亡
英文关键词: Ursodeoxycholic acid (UDCA)  Doxorubicin (DOX)  Myocardium protection  Inflammation  Apoptosis
基金项目:江苏省博士后基金(2018K255C)。
作者单位E-mail
王皓 南京医科大学附属儿童医院检验科 wh@njmu.edu.cn 
夏薇薇 南京医科大学附属儿童医院检验科  
陈红兵 南京医科大学附属儿童医院检验科 chenghb1999@126.com 
摘要点击次数: 60
全文下载次数: 0
中文摘要:
      目的 探讨熊去氧胆酸(UDCA)对阿霉素(DOX)诱导的 H9c2 心肌细胞损伤的影响及机制。方法 体外培养H9c2 细胞, 1μM DOX和不同浓度UDCA处理H9c2,CCK-8 法测定细胞活力;实时定量聚合酶链反应检测心肌细胞凋亡分子Bax及炎症因子IL-1b,IL-6的表达;Western blotting 检测UDCA对DOX诱导的心肌细胞凋亡相关蛋白Bax,Bcl2,Caspase3表达水平变化。结果 与对照组相比,DOX组心肌细胞活力减弱;炎症因子IL-1b,IL-6表达上调;促凋亡分子Bax, cleaved Caspase3表达增多;抑制凋亡蛋白Bcl2下调(P < 0.05)。与DOX组相比,UDCA+DOX组显著恢复心肌细胞活力;炎症因子IL-1b,IL-6表达下调;促凋亡分子Bax, cleaved Caspase3下调;抑制凋亡蛋白Bcl2表达上调(P < 0.05)。结论 UDCA能缓解DOX诱导的H9c2心肌细胞损伤,其机制可能与抑制炎症及凋亡有关。本研究为阿霉素心肌毒性的防治提供新的实验基础及理论依据。
英文摘要:
      ABSTRACT Objective: To investigate the effect of UDCA on doxorubicin (DOX)-induced cardiotoxicity in H9c2 cardiomyocytes and the mechanisms. Methods:The H9c2 cardiomyocytes were treated with doxorubicin with or without UDCA of different doses. The cell viability was measured by CCK-8 assay, and the inflammatory factors were examined by quantitative real-time polymerase chain reaction(qRT-PCR). As for apoptosis, Western blotting, qRT-PCR were used to analyze. Results: Compared with control group, the viability of H9c2 cells, the anti-apoptotic protein Bcl2 were decreased (P < 0.05). Additionally, the release of inflammatory factors (IL-1b,IL-6), apoptotic molecules (Bax and Cleaved Caspase3) was increased (P < 0.05). Compared with doxorubicin group, UDCA+DOX group restored the cell viability, ameliorated the release of inflammatory factors (IL-1b,IL-6), inhibited pro-apoptotic molecules (Bax and cleaved Caspase3) and apoptotic cells,promoted anti-apoptotic molecules Bcl2 as well (P < 0.05). Conclusions: UDCA suppresses doxorubicin-induced injury in H9c2 cardiomyocytes by reducing inflammation and apoptosis, which provides a pivotal theoretical basis for the clinical application of UDCA in the prevention and treatment of doxorubicin-induced cardiotoxicity.
View Fulltext   查看/发表评论  下载PDF阅读器
关闭