Karabulut Derya, Ulusoy Hasan Basri, Kaymak Emin, Sönmez Mehmet Fatih
Department of Histology and Embryology, Faculty of Medicine, Erciyes University; Kayseri-Turkey.
Anatol J Cardiol. 2016 May;16(5):310-5. doi: 10.5152/akd.2015.6252. Epub 2015 May 5.
Diabetes mellitus causes a decrease in cardiac output, arterial blood pressure, and heart rate. In this study, we aimed to investigate, at the molecular level, the effect of nitric oxide synthase (NOS) on heart pathology in type 1 diabetes and look at the therapeutic effect of pentoxifylline on this pathology.
In this experimental study, 50 Wistar albino male rats were used. The rats were divided into 5 groups: group C, control; group D, only diabetes; group D+PI and D+PII, diabetes + pentoxifylline; group P, only pentoxifylline. Group D+PI rats received 50 mg/kg/day pentoxifylline over two months. However, group D+PII rats received saline in the first month and 50 mg/kg/day of pentoxifylline over the following month. At the end of two months, NOS expressions in heart tissue were assessed through immunohistochemistry analysis. The data were compared by one-way ANOVA.
At the end of the experiments, there was increased cytoplasmic vacuolization, myofibrillar loss, cytoplasmic eosinophilia, and degeneration of cardiomyocytes; nNOS and iNOS expressions in group D decreased compared with that in group C. In group D+PI and group D+PII, nNOS and iNOS expressions improved compared with group D.
As a result, we found that diabetes, a known chronic disease, causes serious damage in heart tissue. NOS plays a role in this damage, and pentoxifylline aided in improving nNOS and iNOS expression in this damage.
糖尿病会导致心输出量、动脉血压和心率下降。在本研究中,我们旨在从分子水平研究一氧化氮合酶(NOS)对1型糖尿病心脏病理的影响,并观察己酮可可碱对该病理的治疗作用。
在本实验研究中,使用了50只雄性Wistar白化大鼠。将大鼠分为5组:C组,对照组;D组,仅患糖尿病组;D + PI组和D + PII组,糖尿病 + 己酮可可碱组;P组,仅用己酮可可碱组。D + PI组大鼠在两个月内接受50 mg/kg/天的己酮可可碱。然而,D + PII组大鼠在第一个月接受生理盐水,在接下来的一个月接受50 mg/kg/天的己酮可可碱。在两个月结束时,通过免疫组织化学分析评估心脏组织中NOS的表达。数据通过单因素方差分析进行比较。
实验结束时,出现细胞质空泡化增加、肌原纤维丧失、细胞质嗜酸性粒细胞增多和心肌细胞变性;与C组相比,D组中nNOS和iNOS的表达降低。在D + PI组和D + PII组中,与D组相比,nNOS和iNOS的表达有所改善。
结果,我们发现糖尿病这种已知的慢性病会对心脏组织造成严重损害。NOS在这种损害中起作用,而己酮可可碱有助于改善这种损害中nNOS和iNOS的表达。