| 王 皓,夏薇薇,龙广凤,杨大恒,裴知音,陈红兵.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[J].现代生物医学进展英文版,2021,(3):418-423. |
| 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 |
| Received:July 28, 2020 Revised:August 21, 2020 |
| DOI：10.13241/j.cnki.pmb.2021.03.004 |
| 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:江苏省博士后科研基金项目（2018K255C） |
|
| Hits: 1157 |
| Download times: 664 |
| 中文摘要: |
| 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，1 μM 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-1β、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-1β，IL-6表达上调；促凋亡分子Bax和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-1β、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 Ursodeoxycholic Acid (UDCA) on doxorubicin (DOX)-induced cardiotoxicity in H9c2 cardiomyocytes and the mechanisms. Methods: The H9c2 cardiomyocytes were treated with DOX 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-1β, IL-6), apoptotic molecules(Bax and Cleaved Caspase3) was increased(P<0.05). Compared with DOX group, UDCA+DOX group restored the cell viability, ameliorated the release of inflammatory factors(IL-1β, IL-6), inhibited pro-apoptotic molecules(Bax and Cleaved Caspase3), promoted anti-apoptotic molecules Bcl2 as well (P<0.05). Conclusion: UDCA suppresses DOX-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 DOX-induced cardiotoxicity. |
|
View Full Text
View/Add Comment Download reader |
| Close |
