李红艳, 赵思涵, 梅显运, 陈政, 李旭光, 孙芳云. 甘松新酮对H9C2心肌细胞低氧损伤的作用及其机制[J]. 华南师范大学学报(自然科学版), 2021, 53(2): 51-58. doi: 10.6054/j.jscnun.2021026
引用本文: 李红艳, 赵思涵, 梅显运, 陈政, 李旭光, 孙芳云. 甘松新酮对H9C2心肌细胞低氧损伤的作用及其机制[J]. 华南师范大学学报(自然科学版), 2021, 53(2): 51-58. doi: 10.6054/j.jscnun.2021026
LI Hongyan, ZHAO Sihan, MEI Xianyun, CHEN Zheng, LI Xuguang, SUN Fangyun. The Effect of Nardosinone on Hypoxic Injury of H9C2 Cardiomyocytes and Its Mechanism[J]. Journal of South China Normal University (Natural Science Edition), 2021, 53(2): 51-58. doi: 10.6054/j.jscnun.2021026
Citation: LI Hongyan, ZHAO Sihan, MEI Xianyun, CHEN Zheng, LI Xuguang, SUN Fangyun. The Effect of Nardosinone on Hypoxic Injury of H9C2 Cardiomyocytes and Its Mechanism[J]. Journal of South China Normal University (Natural Science Edition), 2021, 53(2): 51-58. doi: 10.6054/j.jscnun.2021026

甘松新酮对H9C2心肌细胞低氧损伤的作用及其机制

The Effect of Nardosinone on Hypoxic Injury of H9C2 Cardiomyocytes and Its Mechanism

  • 摘要: 以氯化钴(CoCl2)构建H9C2心肌细胞低氧损伤模型,研究Nar在其中的作用及机制. CCK-8试剂盒检测细胞活力,流式细胞仪测细胞凋亡,以自噬抑制剂3-MA预作用细胞探讨Nar对自噬的影响,Western Blot检测Beclin-1、LC3II/LC3I、P62、Bax、Bcl-2和Caspase-3蛋白表达,分光光度计测定乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、丙二醛(MDA)和肌酸激酶(CK)含量. 结果显示:CoCl2 (500 μmol/L)可抑制约50 %细胞生长,而Nar (50 μmol/L)预处理显著减轻了CoCl2 (500 μmol/L)诱导的细胞凋亡;另外,Nar通过增加LC3II/LC3I和Beclin-1表达及促进P62降解激活了自噬,但3-MA预作用逆转了该过程;3-MA预作用同时逆转了Nar对CoCl2造成的H9C2细胞凋亡和氧化损伤的保护作用. 研究表明:Nar在心肌细胞低氧损伤中以诱导自噬抑制凋亡的方式保护心肌细胞,Nar可能成为治疗低氧性心脏病的潜在药物.

     

    Abstract: The model of hypoxic injury of H9C2 cardiomyocytes was established with cobalt chloride (CoCl2) to study the role of Nardosinone (Nar) in it and its mechanism. CCK-8 kit was used to detect cell viability and flow cytometry was used to detect apoptosis. Autophagy inhibitor 3-MA was used to pretreat cells to evaluate the effect of Nar on autophagy. The expressions of Beclin-1, LC3II/LC3I, P62, Bax, Bcl-2 and Caspase-3 were detected with Western Blot, and the contents of lactate dehydrogenase (LDH), superoxide dismutase (SOD), malondialdehyde (MDA) and creatine kinase (CK) were measured with spectrophotometer. The results showed that CoCl2(500 μmol/L) inhibited the growth of H9C2 cells by about 50% while the pretreatment with Nar(50 μmol/L) significantly alleviated CoCl2-induced cell apoptosis. In addition, Nar promoted P62 degradation and increased the expressions of LC3II/LC3I and Beclin-1, which were reversed with 3-MA pretreatment. At the same time, pretreatment with 3-MA reversed the protective effects of Nar on CoCl2-caused H9C2 cell apoptosis and oxidative damage. The results showed that Nar played a protective role in myocardial hypoxic injury by inducing autophagy and inhibiting apoptosis. It was suggested that Nar may be a potential drug for the treatment of hypoxic heart disease.

     

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