Volume 19 Issue 10
Oct.  2021
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Article Navigation >  Chinese Journal of General Practice  > 2021  >  19(10): 1621-1625,1653
QIN Zi-han, CHEN Ying-min, PU Jun. Nuclear receptor corepressor 1 significantly attenuates myocardial infarction injury in mice[J]. Chinese Journal of General Practice, 2021, 19(10): 1621-1625,1653. doi: 10.16766/j.cnki.issn.1674-4152.002126
Citation: QIN Zi-han, CHEN Ying-min, PU Jun. Nuclear receptor corepressor 1 significantly attenuates myocardial infarction injury in mice[J]. Chinese Journal of General Practice, 2021, 19(10): 1621-1625,1653. doi: 10.16766/j.cnki.issn.1674-4152.002126
shu

Nuclear receptor corepressor 1 significantly attenuates myocardial infarction injury in mice

doi: 10.16766/j.cnki.issn.1674-4152.002126

  • Department of Cardiology, Renji Hospital, School of Medicine, Shanghai .Jiao Tong University ，Shanghai 200127,China

Funds:

 81930007

  • Received Date: 2021-01-28
    Available Online: 2022-02-15
    Abstract
  •   Objective   To explore the effect of nuclear receptor corepressor 1 (NCoR1) derived from cardiomyocytes on myocardial infarction injury in mice.   Methods   Cardiomyocyte-specific NCoR1 knockout mice were constructed and divided into the sham operation wild-type group, sham operation gene knockout group, myocardial infarction wild-type group and myocardial infarction gene knockout group, with 50 mice in each group. The survival rate and cardiac function level of mice in each group at 28 days of myocardial infarction were statistically analysed. Pathological staining was used to determine the infarct area and fibrosis degree. The levels of serum myocardial enzymes (creatine kinase MB, lactate dehydrogenase) and inflammation indicators (tumor necrosis factor-α, interleukin-6) were determined.   Results   Compared with wild-type mice, the knockout group mice had lower survival rate, significantly decreased left ventricular ejection fraction [(30.39±5.13)% vs. (9.46±2.10)%] and left ventricular shortening fraction [(14.62±2.69)% vs. (4.26±0.96)%], and significantly increased left ventricular volume [(101.50±14.07)μL vs. (197.50±22.41)μL, all P < 0.05]. Small animal PET/CT indicated that wild-type mice had higher intake of 18F-FDG after myocardial infarction [(2.74±0.06)MBq vs. (1.60±0.03)MBq] and degree of infarction [(36.22±0.86)% vs. (47.17±1.27)%] and degree of fibrosis [(32.70±0.85)% vs. (46.38±1.31)%, all P < 0.05]. Serological indicators showed that the myocardial damage of knockout mice was more severe, and the level of inflammation was higher (all P < 0.05).   Conclusion   NCoR1 in cardiomyocytes plays an important protective role in myocardial infarction in mice.

     

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