[1]李登科 张伟 黄从新.黄芩苷通过调节Nrf2/HO-1信号通路减轻阿霉素诱导的H9c2细胞毒性[J].心血管病学进展,2024,(5):457.[doi:10.16806/j.cnki.issn.1004-3934.2024.05.017]
　LI Dengke,ZHANG Wei,HUANG Congxin.Baicalin Reduces Doxorubicin Induced H9c2 Cell Toxicity by Regulating the Nrf2/HO-1 Signaling Pathway[J].Advances in Cardiovascular Diseases,2024,(5):457.[doi:10.16806/j.cnki.issn.1004-3934.2024.05.017]
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黄芩苷通过调节Nrf2/HO-1信号通路减轻阿霉素诱导的H9c2细胞毒性()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2024年5期
页码:
457
栏目:
论著
出版日期:
2024-05-25

文章信息/Info

Title:
Baicalin Reduces Doxorubicin Induced H9c2 Cell Toxicity by Regulating the Nrf2/HO-1 Signaling Pathway
作者:
李登科 张伟 黄从新
(武汉大学人民医院心内科 武汉大学心血管病研究所 心血管病湖北省重点实验室,湖北 武汉 430060 )
Author(s):
LI Dengke; ZHANG Wei; HUANG Congxin
(Department of Cardiology,Renmin Hospital of Wuhan University,Cardiovascular Research Institute,Wuhan University,Hubei Key Laboratory of Cardiology,Wuhan 430060 ,Hubei,China)
关键词:
阿霉素; H9c2细胞; 黄芩苷; 氧化应激; 凋亡
Keywords:
Doxorubicin; H9c2 cell; Baicalin; Oxidative stress; Apoptosis
DOI:
10.16806/j.cnki.issn.1004-3934.2024.05.017
摘要:
目的 探讨黄芩苷对阿霉素诱导的H9c2细胞毒性的影响及内在机制。方法 采用50μmol/L黄芩苷预处理H9c2细胞24 h，然后1μmol/L Dox处理H9c2细胞24 h建立体外阿霉素心肌毒性模型。采CCK8法检测细胞活力；收集细胞上清检测各组心肌损伤标志物乳酸脱氢酶(LDH)、心肌肌钙蛋白I（cTnI）和肌酸激酶同工酶(CK-MB)的水平及氧化应激相关指标超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-PX）和丙二醛（MDA）的水平；使用DHE试剂盒检测各组活性氧（ROS）的含量；使用TUNEL染色检测各组细胞凋亡水平，RT-qPCR和Western blot实验用于检测氧化应激和凋亡相关分子的表达水平。结果 与Dox组相比，黄芩苷能够提高H9c2细胞活力，降低LDH、cTnI、CK-MB水平；DHE染色显示黄芩苷能够减少ROS的生成，增加SOD、GSH-PX的活性，降低MDA的含量；TUNEL染色结果显示黄芩苷能够减少阳性细胞数量；RT-qPCR和Western blot检测显示黄芩苷能够上调Nrf2、HO-1、SOD2、Bcl-2的表达，降低Cleaved-caspase 3和Bax的表达。然而，Nrf2的特异性抑制剂ML385可逆转黄芩苷引起的上述变化。结论 黄芩苷通过上调Nrf2/HO-1信号通路减轻氧化应激和凋亡，减轻阿霉素诱导的H9c2细胞毒性。
Abstract:
Objective This study aims to investigate the effect and underlying mechanism of baicalin on doxorubicin-induced H9c2 cell toxicity. Methods H9c2 cells were pretreated with 50 μmol/L baicalin for 24 h ,followed by treatment with 1 μmol/L Dox for 24 h to establish an in vitro model of doxorubicin-induced myocardial toxicity. Cell viability was assessed using the CCK8 assay. The levels of lactate dehydrogenase (LDH),cardiac troponin I (cTnI),creatine kinase isoenzyme (CK-MB),as well as oxidative stress-related indicators such as superoxide dismutase (SOD),glutathione peroxidase (GSH-PX),and malondialdehyde (MDA) were measured in the cell supernatant of each group. Reactive oxygen species (ROS) content was determined using the DHE assay kit. TUNEL staining was employed to assess cell apoptosis levels in each group. Additionally,RT-qPCR and Western blot experiments were conducted to measure the expression levels of oxidative stress and apoptosis-related molecules. However,ML385,a specific inhibitor of Nrf2,reversed the above changes induced by baicalin. Results Baicalin demonstrated the ability to enhance H9c2 cell viability and decrease LDH ,cTnI,and CK-MB levels compared to the Dox group. DHE staining indicated that baicalin reduced ROS generation,increased SOD and GSH-PX activity,and decreased MDA content. TUNEL staining results revealed a reduction in the number of positive cells with baicalin treatment. RT-qPCR and Western blot analysis showed that baicalin upregulated the expression of Nrf2,HO-1,SOD2,and Bcl-2,while downregulating the expression of Cleaved-caspase 3 and Bax. Conclusion Baicalin alleviates oxidative stress and apoptosis by upregulating the Nrf2/HO-1 signaling pathway ,thereby mitigating doxorubicin-induced H9c2 cell toxicity

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更新日期/Last Update: 2024-06-28