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The protective effects of grape seed procyanidin B2 against asporin mediates glycated low‐density lipoprotein?induced‐cardiomyocyte apoptosis and fibrosis

机译:葡萄籽胰蛋白酶B2对孢子蛋白的保护作用介质糖化低密度脂蛋白的血糖细胞凋亡和纤维化

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Abstract The progression of diabetic cardiomyopathy is related to cardiomyocyte dysfunction and apoptosis. Our previous studies showed that asporin (ASPN) was significantly increased in the myocardium of db/db mice through proteomics, and grape seed procyanidin B2 (GSPB2) significantly inhibited the expression of ASPN in the heart of db/db mice. We report?here that ASPN played a critical role in glycated low‐density lipoproteins (gly‐LDL) induced‐cardiomyocyte apoptosis. We found that gly‐LDL upregulated ASPN expression. ASPN increased H9C2 cardiomyocyte?apoptosis with down‐regulation of Bcl‐2, upregulation of transforming growth factor‐β1, Bax, collagen III, fibronectin, and phosphorylation of smad2 and smad3. However, GSPB2 treatment reversed ASPN‐induced impairments in H9C2 cardiomyocytes. These results provide evidence for the cardioprotective action of GSPB2 against ASPN injury, and thus suggest a new target for fighting against diabetic cardiomyopathy.
机译:糖尿病心肌病的进展与心肌细胞功能障碍和凋亡有关。我们之前的研究表明,通过蛋白质组学,db/db小鼠心肌中的阿司匹林(ASPN)显著增加,葡萄籽原花青素B2(GSPB2)显著抑制db/db小鼠心脏中ASPN的表达。我们报道?在此,ASPN在糖化低密度脂蛋白(gly-LDL)诱导的心肌细胞凋亡中起着关键作用。我们发现甘氨酸-低密度脂蛋白上调了ASPN的表达。ASPN增加H9C2心肌细胞?凋亡与Bcl-2的下调、转化生长因子β1、Bax、III型胶原、纤维连接蛋白的上调以及smad2和smad3的磷酸化有关。然而,GSPB2治疗逆转了ASPN诱导的H9C2心肌细胞损伤。这些结果为GSPB2对ASPN损伤的心脏保护作用提供了证据,从而为对抗糖尿病心肌病提供了新的靶点。

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