乳酸脱氢酶D在阿霉素诱导的心肌细胞损伤中的保护作用研究
首发时间:2026-03-17
摘要:目的:探讨乳酸脱氢酶D(Ldhd)在阿霉素(doxorubicin,DOX)诱导的心肌细胞损伤中的保护作用。方法:建立DOX诱导的AC16和H9C2心肌细胞损伤模型,检测Ldhd在损伤前后的表达水平变化;通过过表达和敲低Ldhd,观察AC16心肌细胞在DOX处理前后活性氧(ROS)水平及线粒体膜电位的变化。结果:(1)Ldhd在DOX诱导的心肌细胞损伤中表达显著上调;(2)过表达Ldhd可显著抑制DOX诱导的ROS升高,并缓解线粒体膜电位的下降;而敲低Ldhd则进一步加剧ROS生成和线粒体膜电位下降。结论:过表达Ldhd可减轻受损心肌细胞的氧化应激反应,保护线粒体功能,提示其在心肌损伤干预及治疗研究中具有潜在价值。
关键词: 乳酸脱氢酶D 阿霉素 心肌细胞损伤 氧化应激 线粒体功能
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Protective Role of D-Lactate Dehydrogenase in Doxorubicin-Induced Cardiomyocyte Injury
Abstract:Aim: Investigation of the protective role of D-lactate dehydrogenase (Ldhd) in doxorubicin (DOX)-induced cardiomyocyte injury. Methods: Cardiomyocyte injury model was established by DOX treatment in AC16 and H9C2 cells and the Ldhd levels were measured before and after the injury. Further, the Ldhd expression was upregulated and downregulated in AC16 via plasmid transient transfection and siRNA interference, respectively, and the effects on the oxidative stress and mitochondrial function were examinedwith live-cell immunofluorescence staining. Results: (1) The Ldhd expression was significantly upregulated by the DOX-induced injury. (2) The DOX treatment resulted in the elevation of ROS production and declination of mitochondrial membrane potential. The overexpression of Ldhd attenuated both the tendencies, while the knockdown worsened both. Conclusions: These findings suggest that Ldhd may contribute to the protection of injured cardiomyocytes, potentially through the suppression of oxidative stress and preservation of mitochondrial function. Further investigation is warranted to explore its relevance as a therapeutic target in cardiac diseases.
Keywords: D-lactate dehydrogenase doxorubicin cardiomyocyte injury oxidative stress mitochondrial function
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乳酸脱氢酶D在阿霉素诱导的心肌细胞损伤中的保护作用研究
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