评估催产素对实验性心力衰竭心肌结构和功能变化的影响

A. D. Starchenko, Yulia V. Liskova, A. A. Stadnikov, A. A. Myasnikova
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摘要

研究旨在评估催产素对实验性心力衰竭(EHF)心肌结构和功能重组的影响。以 Wistar 系成熟雌雄大鼠(36 只)为模型进行心力衰竭实验。从实验的第 7 天开始,每天按每公斤体重 0.5 U 的剂量肌肉注射催产素,连续一周。通过光学显微镜、形态测量和免疫组化(caspase-3、bcl-2、ki-67 蛋白表达)对获得的材料(心脏、左心室心肌)进行研究。研究结果组织学制备的综合分析表明,心力衰竭患者左心室心肌的所有结构(心肌细胞(CMC)、微血管、结缔组织基质)都发生了病理变化。在引入催产素的背景下,心肌细胞和毛细血管的体积密度(VD)会增加,而基质成分的体积密度会降低。催产素对心肌细胞凋亡的抑制作用和对心肌修复过程的激活作用得到了证实:在 EHF 的雌雄动物中,caspase-3 阳性心肌细胞数量减少,表达 bcl-2 和 ki-67 的 CMC 增加。在催产素的影响下,雌性 EHF 患者组的再生和抗凋亡潜能得到了更显著的激活。结论研究获得的全部数据表明,催产素对心衰患者的心肌结构具有保护作用,其特点是刺激血管生成、抑制纤维化和细胞凋亡,以及激活细胞适应性心肌重塑途径。催产素对心肌的生物效应具有性别特异性,这使人们对催产素能系统在心脏中的作用有了新的认识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Evaluation of the effect of oxytocin on structural and functional changes of the myocardium in experimental heart failure
The aim of the study was to evaluate the effect of oxytocin on the structural and functional reorganization of the myocardium in experimental heart failure (EHF) Material and methods. Heart failure was modeled on mature rats of both sexes of the Wistar line (n=36). From the 7th day of the experiment, oxytocin was administered to animals with EHF at a dose of 0.5 U / kg of body weight daily intramuscularly for a week. The obtained material (heart, left ventricular (LV) myocardium) was studied by light microscopy, morphometry, and immunohistochemistry (expression of caspase-3, bcl-2, ki-67 proteins). Results. A comprehensive analysis of histological preparations showed that in heart failure, pathological changes occur in all structures of the LV myocardium (in cardiomyocytes (CMC), vessels of the microvasculature, connective tissue stroma). Against the background of the introduction of oxytocin, there is an increase in the volume density (VD) of cardiac myocytes, capillaries and a decrease in the VD of stromal components. Oxytocin inhibition of the proapoptotic dominant and activation of reparative processes in the myocardium were established: there was a decrease in the number of caspase-3-positive cardiac myocytes and an increase in CMC expressing bcl-2 and ki-67 in animals of both sexes with EHF. Under the influence of oxytocin, a more significant activation of regenerative and antiapoptotic potential was revealed in the group of females with EHF. Conclusion. The totality of the data obtained as a result of the study indicates the cardioprotective effect of oxytocin on myocardial structures in heart failure, characterized by stimulation of vasculogenesis, inhibition of fibrosis and apoptosis, and activation of cellular adaptive myocardial remodeling pathways. The biological effect of oxytocin on the myocardium is characterized by gender-specific features of the realization of its effects, which gives a new understanding of the role of the oxytocinergic system in the heart.
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