孙晓, 高星, 肖黎明, 杨韩, 叶菁, 袁铭. Perilipin 5缺失导致线粒体功能异常加剧肥胖小鼠心肌的氧化应激损伤[J]. 心脏杂志, 2021, 33(1): 11-16. DOI: 10.12125/j.chj.202010013
    引用本文: 孙晓, 高星, 肖黎明, 杨韩, 叶菁, 袁铭. Perilipin 5缺失导致线粒体功能异常加剧肥胖小鼠心肌的氧化应激损伤[J]. 心脏杂志, 2021, 33(1): 11-16. DOI: 10.12125/j.chj.202010013
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    Xiao SUN, Xing GAO, Li-ming XIAO, Han YANG, Jing YE, Ming YUAN. Lack of Perilipin 5 results in abnormality in mitochondrial functions and aggravates oxidative stress injury of obesity cardiomyopathy[J]. Chinese Heart Journal, 2021, 33(1): 11-16. DOI: 10.12125/j.chj.202010013
    Citation: Xiao SUN, Xing GAO, Li-ming XIAO, Han YANG, Jing YE, Ming YUAN. Lack of Perilipin 5 results in abnormality in mitochondrial functions and aggravates oxidative stress injury of obesity cardiomyopathy[J]. Chinese Heart Journal, 2021, 33(1): 11-16. DOI: 10.12125/j.chj.202010013
    shu

    Perilipin 5缺失导致线粒体功能异常加剧肥胖小鼠心肌的氧化应激损伤

    Lack of Perilipin 5 results in abnormality in mitochondrial functions and aggravates oxidative stress injury of obesity cardiomyopathy

      摘要
    • 摘要:
        目的  探讨Perilipin 5缺失是否会导致小鼠的线粒体功能异常，从而加剧肥胖小鼠心肌的氧化应激损伤。
        方法  对各组小鼠心脏进行超声分析，对心肌组织进行HE染色观察心肌肥厚程度，检测心肌组织中丙二醛（MDA）含量和超氧化物歧化酶（SOD）水平，Western blot检测心肌组织线粒体以及胞质内 Cytochrome C蛋白的表达水平。
        结果  与ob/ob小鼠对比，ob/ob/Plin5-/-小鼠心脏LVEF、LVIDd进一步降低（均P<0.05），LVIDs进一步增大（P<0.01），心肌细胞横截面积（P<0.05）和LVPWd进一步增大（P<0.05），MDA进一步上升（P<0.01），SOD进一步下降（P<0.05），心肌线粒体 Cytochrome C蛋白表达明显降低（P<0.01），胞质中 Cytochrome C蛋白表达明显升高（P<0.01）。
        结论  Plin5的缺失可能通过干扰线粒体功能，加剧肥胖小鼠心肌的氧化应激损伤，进而引起小鼠心脏功能的进一步损害。

       

      Abstract:
        AIM  To investigate whether Perilipin 5 deficiency may cause abnormal mitochondrial functions in mice, thus exacerbating oxidative stress injury of the myocardium in obesity mice.
        METHODS  For each group of mice, an ultrasound analysis on cardiac function was conducted and the myocardial tissue was observed for myocardial hypertrophy using HE staining method. Malondialdehyde (MDA) and superoxide dismutase (SOD) in myocardial tissue were tested and the secretion levels of mitochondria and Cytochrome C protein in mitochondria and cytoplasm of myocardial tissue were detected using Western blot method.
        RESULTS  Compared with those of ob/ob mice, Compared with ob/ob mice, the heart LVEF and LVIDd of ob/ob/Plin5-/- mice were further decreased (both P<0.05), LVIDs were further decreased (P<0.01), further increase of cross-sectional area of myocardial cells (P<0.05) and LVPWD (P<0.05), MDA further increased (P<0.01), SOD decreased further (P<0.05). The expression of Cytochrome C protein in myocardial mitochondria was significantly decreased (P<0.01), the expression of Cytochrome C protein in cytoplasm increased significantly (P<0.01).
        CONCLUSION  Plin5 deficiency may aggravate oxidative stress injury of myocardium through interfering with mitochondrial functions, thus causing damage to heart functions in mice.

       

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