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    罗　燕, 王　徽, 岳　洋, 等. 基于代谢组学研究电击伤所致小鼠心肌损伤的效应研究[J]. 广西医科大学学报, 2024, 1(X): 1-7. DOI：.
    引用本文: 罗　燕, 王　徽, 岳　洋, 等. 基于代谢组学研究电击伤所致小鼠心肌损伤的效应研究[J]. 广西医科大学学报, 2024, 1(X): 1-7. DOI：.
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    LUO Y, WANG H, YUE Y, et al. Study on the effect of myocardial injury induced by electrical injury in mice based on metabolomics[J]. Journal of Guangxi medical university, 2024, 1(X): 1-7. DOI：.
    Citation: LUO Y, WANG H, YUE Y, et al. Study on the effect of myocardial injury induced by electrical injury in mice based on metabolomics[J]. Journal of Guangxi medical university, 2024, 1(X): 1-7. DOI：.
    shu

    基于代谢组学研究电击伤所致小鼠心肌损伤的效应研究

    Study on the effect of myocardial injury induced by electrical injury in mice based on metabolomics

      摘要
    • 摘要:
      目的 基于代谢组学技术研究电击伤所致小鼠心肌损伤，并找出心脏代谢组学差异代谢物和差异代谢途径。
      方法 40只C57BL/6J小鼠随机分为对照组和电击组，每组20只。对照组仅用电击装置的声光刺激小鼠头部5 s，电击组用电击装置持续电击小鼠头部5 s；然后用眼球取血法收集两组小鼠血液并检测血清脑钠肽（BNP）和心肌酶谱指标；心脏灌注法取心脏组织行石蜡切片和心肌苏木精—伊红染色 （HE）染色、普鲁士蓝染色和麦胚凝集素染色，观察心肌病理改变；不灌注取小鼠心脏组织行代谢组学检测。
      结果 与对照组比较，电击组小鼠血清BNP和乳酸脱氢酶1（LDH1）含量升高（P＜0.05）；麦胚凝集素染色显示心肌细胞平均细胞面积明显增大〔（1.64±0.23）vs.（1.93±0.14），P＜0.01〕；心脏代谢组学分析以OPLS-DA VIP＞1 和 P＜0.05为标准筛选到6个表达上调的差异代谢物和13个表达下调的差异代谢物，KEGG通路富集分析显示差异代谢物主要影响癌症中心碳代谢，丙氨酸、天冬氨酸和谷氨酸代谢等代谢途径。
      结论 电击伤可导致小鼠心肌损伤，主要表现为血清BNP、LDH1含量升高，心肌细胞肥大以及以癌症中心碳代谢为主的心肌代谢途径异常。

       

      Abstract:
      Objective To study myocardial injury induced by electrical injury in mice based on metabolomics, and to find out the differential metabolites and pathways in cardiac metabolism omics.
      Methods Forty C57BL/6J mice were randomly divided into control group and electric shock group, with 20 mice in each one. The mouse heads in the control group were only stimulated with the sound and light of the electric shock device for 5s, and those in the electric shock group were continuously shocked with the electric shock device for 5s. Then the blood of two groups was collected by the method of eyeball blood collection and the serum brain natriuretic peptide (BNP) and myocardial enzyme spectrum were detected. Cardiac tissue was taken by heart perfusion method for paraffin sections and myocardial hematoxylin-eosin (HE) staining, Prussian blue staining and wheat germ agglutinin staining were performed to observe the pathological changes of the myocardium. The cardiac tissue of mice without perfusion was examined by metabolomics.
      Results Compared with the control group, the contents of serum BNP and lactate dehydrogenase 1 (LDH1) of mice in the electric shock group were increased (P＜0.05). The wheat germ agglutinin staining showed that the mean cell area of cardiomyocytes was increased significantly (1.64±0.23) vs. (1.93±0.14), P＜0.01. Cardiometabolic analysis was performed with the criterion of OPLS-DA VIP＞1 and P＜0.05 for screening differential metabolites. Six up-regulated differential metabolites and 13 up-regulated differential metabolites were screened. The results of KEGG pathway enrichment analysis showed that differential metabolites mainly affected cancer-related pathways such as center carbon metabolism in cancer, as well as alanine, aspartic acid and glutamate metabolism.
      Conclusion Electrical injury can lead to myocardial injury in mice, mainly manifested as increased serum BNP and LDH1 content, cardiomyocyte hypertrophy and abnormal myocardial metabolic pathway, mainly centered on center carbon metabolism in cancer.

       

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