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A Pilot Study of Matrix Metalloproteinases on the Model of Daunorubicin-induced Cardiomyopathy in Rabbits

机译:柔红霉素诱导的心肌病模型中基质金属蛋白酶的初步研究

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Matrix metalloproteinases (MMPs), activated by oxidative stress, play a key role during cardiac remodeling. In the present study we aimed to assess the role of MMPs in experimental cardiomyopathy induced by repeated 10-week administration of daunorubicin (3 mg/kg i.v.) to rabbits. In the daunorubicin group, the plasma cardiac troponin T levels (cTnT – a marker of myocardial necrosis) were significantly increased (p<0.05), commencing with the 8th administration compared with the controls. The amount of collagen (an estimate of fibrosis) was also significantly higher in the daunorubicin group (13.39 ± 0.97 mg/g wet weight) compared to the control group (10.03 ± 0.65 mg/g wet weight). In both groups, the LV MMP-activity was observed only in the gelatine substrate in the 70 kDa region (MMP-2), while no MMPs activities were detectable either in the casein or collagen containing zymograms. At the end of the experiment, the MMP- 2 activity was slightly up-regulated (by 16 %) compared with the controls.
机译:氧化应激激活的基质金属蛋白酶(MMP)在心脏重塑中起关键作用。在本研究中,我们旨在评估MMP在实验性心肌病中的作用,该实验性心肌病是通过对兔反复施用柔红霉素(3 mg / kg静脉内)十周诱导的。在柔红霉素组中,与第8次给药相比,血浆心肌肌钙蛋白T水平(cTnT –心肌坏死的标志物)显着增加(p <0.05)。与对照组(10.03±0.65 mg / g湿重)相比,柔红霉素组(13.39±0.97 mg / g湿重)的胶原蛋白含量(估计的纤维化)也明显更高。在两组中,仅在70 kDa区域的明胶底物(MMP-2)中观察到LV MMP活性,而在酪蛋白或含胶原酶的酶谱图中均未检测到MMPs活性。在实验结束时,与对照相比,MMP-2活性略有上调(16%)。

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