张淑苗, 刘银姬, 郭尧涛, 顾晓明, 贾敏, 李娟, 冯娜, 刘亚莉, 雷海录. 钠尿肽嵌合体CNAAC抗大鼠缺血/再灌注心肌损伤的作用[J]. 心脏杂志, 2022, 34(5): 497-501, 509. DOI: 10.12125/j.chj.202111104
    引用本文: 张淑苗, 刘银姬, 郭尧涛, 顾晓明, 贾敏, 李娟, 冯娜, 刘亚莉, 雷海录. 钠尿肽嵌合体CNAAC抗大鼠缺血/再灌注心肌损伤的作用[J]. 心脏杂志, 2022, 34(5): 497-501, 509. DOI: 10.12125/j.chj.202111104
    shu
    Shu-miao ZHANG, Yin-ji LIU, Yao-tao GUO, Xiao-ming GU, Min JIA, Juan LI, Na FENG, Ya-li LIU, Hai-lu LEI. Effect of CNAAC, a new natriuretic pepetide chimera, on myocardial damage caused by ischemia/reperfusion in rats[J]. Chinese Heart Journal, 2022, 34(5): 497-501, 509. DOI: 10.12125/j.chj.202111104
    Citation: Shu-miao ZHANG, Yin-ji LIU, Yao-tao GUO, Xiao-ming GU, Min JIA, Juan LI, Na FENG, Ya-li LIU, Hai-lu LEI. Effect of CNAAC, a new natriuretic pepetide chimera, on myocardial damage caused by ischemia/reperfusion in rats[J]. Chinese Heart Journal, 2022, 34(5): 497-501, 509. DOI: 10.12125/j.chj.202111104
    shu

    钠尿肽嵌合体CNAAC抗大鼠缺血/再灌注心肌损伤的作用

    Effect of CNAAC, a new natriuretic pepetide chimera, on myocardial damage caused by ischemia/reperfusion in rats

      摘要
    • 摘要:
        目的  探讨钠尿肽嵌合体CNAAC在抗缺血/再灌注（ischemia/reperfusion, I/R）心肌损伤中的作用及可能机制。
        方法  将SD大鼠随机分为三组，即假手术组（Sham组）、缺血/再灌注组（I/R组）、缺血/再灌注+CNAAC组（I/R+CNAAC组），缺血30 min，再灌注120 min。再灌注结束后观察并检测各组大鼠心肌组织结构、心肌细胞超微结构、心肌细胞凋亡、体液因子和相关蛋白表达的变化。
        结果  与Sham组相比，I/R组大鼠心肌细胞出现肿胀、炎性浸润，心肌线粒体分裂增加，细胞色素C的表达、心肌细胞凋亡增多（P<0.01），心肌梗死面积、血清LDH、CK-MB和cTnT的水平显著增加（P<0.01），心肌PI3K、磷酸化Akt（Ser473）表达显著减少（P<0.01）；与I/R组相比，I/R+CNAAC组大鼠心肌细胞炎性浸润减少、心肌排列整齐，心肌线粒体分裂被抑制，细胞色素C的表达、心肌细胞凋亡减少（P<0.01），心肌梗死面积降低（P<0.01），血清中LDH、CK-MB、cTnT的水平下降（P<0.01），心肌PI3K、磷酸化Akt的表达显著增加（P<0.01）。
        结论  CNAAC具有上调PI3K/Akt信号通路以及明显改善心肌缺血/再灌注大鼠心肌损伤的作用。

       

      Abstract:
        AIM   To study the effect of CNAAC, a natriuretic peptide chimera, on myocardial damage caused by ischemia/reperfusion.
        METHODS   SD rats were randomly divided into three groups: sham, ischemia/reperfusion (I/R) and I/R + CNAAC groups. After occlusion of the left anterior descending coronary artery (LAD) using 6-0 silk suture for 30 min, the slipknot was released and the animal received 120 min of reperfusion. Sham group underwent the same operation procedures except that the LAD was ligated. HE staining was adopted to observe the pathological changes, transmission electron microscope was employed to observe the structure of mitochondrial morphology and TUNEL kit was used to detect myocardial apoptosis. TTC staining was used to analyze the infarct size, Elisa kits were adopted to measure humoral factors and Western blotting was used to examine the expression of related proteins.
        RESULTS   Compared with the sham group, the I/R group exhibited swelling and inflammatory infiltration in cardiomyocytes. The mitochondrial fission, the expression of cytochrome C and the myocardial apoptosis percentage were increased (P<0.01). The infarct size, the LDH, CK-MB and cTnT levels in serum were also increased (P<0.01). The expressions of PI3K and phosphorylated Akt (Ser 473) were decreased (P<0.01). Compared with the I/R group, the I/R+CNAAC group revealed decreased inflammatory infiltration in cardiomyocytes. The mitochondrial fission was inhibited and the expression of cytochrome C and the myocardial apoptosis percentage were decreased (P<0.01). The infarct size, abnormal LDH, CK-MB and cTnT levels in serum were also decreased (P<0.01). The expressions of PI3K and phosphorylated Akt (Ser 473) were increased (P<0.01).
        CONCLUSION   CNAAC up-regulates PI3K/Akt signaling pathway and ameliorates myocardial damage caused by ischemia/reperfusion.

       

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