[1]郭红豆 蒋凌 罗顺祥 陈甘潇 林佳仪 林奕帆 徐尚华.小白菊内酯对多柔比星诱导的H9c2心肌细胞损伤保护作用的相关机制研究[J].心血管病学进展,2024,(7):666.[doi:10.16806/j.cnki.issn.1004-3934.2024.07.019]
　GUO HongdouJIANG Lin,LUO Shunxiang,CHEN Ganxiao,et al.Study on the Protective Effects and Mechanisms of Parthenolide Against Doxorubicin-Induced H9c2 Cardiomyocyte Injury[J].Advances in Cardiovascular Diseases,2024,(7):666.[doi:10.16806/j.cnki.issn.1004-3934.2024.07.019]
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小白菊内酯对多柔比星诱导的H9c2心肌细胞损伤保护作用的相关机制研究()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2024年7期
页码:
666
栏目:
论著
出版日期:
2024-07-25

文章信息/Info

Title:
Study on the Protective Effects and Mechanisms of Parthenolide Against Doxorubicin-Induced H9c2 Cardiomyocyte Injury
作者:
郭红豆1; 2 蒋凌1 罗顺祥1 陈甘潇1 林佳仪1 林奕帆1 徐尚华1
(1.福建医科大学附属南平第一医院心血管内科,福建 南平 353000;2.武威市人民医院心血管内科,甘肃 武威 733000)
Author(s):
GUO Hongdou1; 2JIANG Lin1; LUO Shunxiang1; CHEN Ganxiao1; LIN Jiayi 1; LIN Yifan1;  XU Shanghua 1
(1.Department of Cardiology,Affiliated Nanping First Hospital,Fujian Medical University,Nanping 353000 ,Fujian,China; 2. Department of Cardiology,Wuwei People ’s Hospital,Wuwei 733000 ,Gansu,China)
关键词:
小白菊内酯; 多柔比星; 心肌细胞; Nrf2/HO-1信号通路; 细胞凋亡
Keywords:
Parthenolide; Doxorubicin; H9c2 cardiomyocytes; Nrf2/HO-1 pathway; Apoptosis
DOI:
10.16806/j.cnki.issn.1004-3934.2024.07.019
摘要:
目的 探索小白菊内酯（PTL）对多柔比星（DOX）诱导的心肌损伤的保护机制及机制。方法 培养H9c2大鼠心肌细胞，应用CCK-8法确定DOX和PTL的最佳作用浓度。将H9c2大鼠心肌细胞分为对照组、PTL组、DOX组及DOX+PTL组进行相应处理，DCFH-DA染色流式细胞仪检测细胞内活性氧水平，Annexin V-FITC/PI染色流式细胞术检测细胞内凋亡比例，蛋白质印迹法检测核转录因子红系2相关因子2（Nrf2）、血红素氧合酶1（HO-1）、Bax和Bcl-2蛋白的表达。结果 检测0.5～5.0 ?mol/L浓度梯度的DOX处理大鼠H9c2心肌细胞24 h后，细胞活力下降，并且呈现剂量依赖性 (P＜0.05)，其中1.0 ?mol/L DOX可引起H9c2细胞活力降至53.0% ±0.4%。5.0 ?mol/L PTL预处理H9c2细胞3 h后可显著增加DOX引起的细胞活力（P＜0.05）。与对照组相比，在DOX组的H9c2心肌细胞中Nrf2、HO-1及Bcl-2蛋白表达显著下降，Bax蛋白表达显著增加（P＜0. 05），氧化应激水平、细胞凋亡比例增多（P＜0. 05）；与DOX组相比，PTL预处理显著增加了DOX处理的H9c2心肌细胞中Nrf2、HO-1、Bcl-2蛋白表达，降低Bax蛋白表达（P＜0. 05），并减少氧化应激水平、细胞凋亡率（P＜0. 05）。结论 PTL缓解DOX引起的H9c2心肌细胞损伤，可能与激活Nrf2/HO-1通路、抑制Bcl-2/Bax通路有关。
Abstract:
Objective To investigate the protective mechanism of parthenolide (PTL) against doxorubicin (DOX)-induced myocardial injury. Methods Rat H9c2 cardiomyocyte s were cultured ,and then the optimal concentration of DOX and PTL was determined by CCK-8 assay. Subsequently,Rat cardiomyocyte H9c2 cells were randomly divided into control group,PTL group,DOX group and DOX+PTL group. Intracellular ROS levels were detected with DCFH-DA using a flow cytometer and the apoptotic cells were measured with Annexin V-FITC/PI staining kit by flow cytometry analysis. Western blot was employed to detect the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2),heme oxygenase-1 (HO-1),Bax and Bcl-2. Results The cell viability of H9c2 cardiomyocytes exposed to 0.5～5.0 ?mol/L DOX for 24?h decreased in a dose-dependent effect ( P＜0.05),and 1.0 ?mol/L DOX could reduce the viability of H9c2 cells to 53.0% ±0.4%. The cell viability of H9c2 cardiomyoctyes pretreated with 5.0 ?mol/L PTL for 3 h before exposure to 1.0 ?mol/L DOX for 24 h was significantly increased (P＜0.05). The protein expression levels of Nrf2,HO-1 and Bcl-2 were decreased significantly comparing with the control group while proapoptoic protein Bax was increased markly (P＜0.05),and the level of oxidative stress and the proportion of apoptosis were increased by DOX (P＜0.05). Contrasted with DOX group,pretreatment with PTL could significantly increase the expression levels of Nrf2,HO-1 and Bcl-2 protein,and reduce the expression level of Bax (P＜0.05),and decrease the degree of oxidative stress and apoptosis rate of DOX-induced H9c2 cardiomyocytes (P＜0.05). Conclusion PTL alleviates DOX-induced injury of H9c2 cardiomyocytes which was associated with activation of Nrf2/HO-1 pathway and inhibition of Bcl-2/Bax signaling pathway

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更新日期/Last Update: 2024-08-09