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| 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)。 |
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| 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. |
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