Sziva Réka Eszter, Fontányi Zoltán, Pál Éva, Hadjadj Leila, Monori-Kiss Anna, Horváth Eszter Mária, Benkő Rita, Magyar Attila, Heinzlmann Andrea, Benyó Zoltán, Nádasy György L, Várbíró Szabolcs
Department of Obstetrics and Gynaecology, Semmelweis University, Üllői Street 78/a, 1082 Budapest, Hungary.
Institute of Translational Medicine, Semmelweis University, Tűzoltó Street 37-47, 1094 Budapest, Hungary.
Antioxidants (Basel). 2020 Oct 15;9(10):997. doi: 10.3390/antiox9100997.
Several reports prove interconnection between vitamin D (VD) deficiency and increased cardiovascular risk. Our aim was to investigate the effects of VD status on biomechanical and oxidative-nitrative (O-N) stress parameters of coronary arterioles in rats.
4-week-old male Wistar rats were divided into a control group (11 animals) with optimal VD supply (300 IU/kgbw/day) and a VD-deficient group (11 animals, <5 IU/kg/day). After 8 weeks, coronary arteriole segments were prepared. Geometrical, elastic, and biomechanical characteristics were measured by in vitro arteriography. O-N stress markers were investigated by immunohistochemistry.
Inner radius decreased; wall thickness and wall-thickness/lumen diameter ratio increased; tangential wall stress and elastic modulus were reduced in VD-deficient group. No difference could be found in wall-cross-sectional area, intima-media area %. While the elastic elements of the vessel wall decreased, the α-smooth muscle actin (α-SMA) immunostaining intensity showed no changes. Significant elevation was found in the lipid peroxidation marker of 4-hidroxy-2-nonenal (HNE), while other O-N stress markers staining intensity (poly(ADP)ribose, 3-nitrotyrosine) did not change.
Inward eutrophic remodeling has developed. The potential background of these impairments may involve the initial change in oxidative damage markers (HNE). These mechanisms can contribute to the increased incidence of the cardiovascular diseases in VD deficiency.
多项报告证实维生素D(VD)缺乏与心血管风险增加之间存在关联。我们的目的是研究VD状态对大鼠冠状动脉小动脉生物力学和氧化-硝化(O-N)应激参数的影响。
将4周龄雄性Wistar大鼠分为对照组(11只动物),给予最佳VD供应(300 IU/kgbw/天)和VD缺乏组(11只动物,<5 IU/kg/天)。8周后,制备冠状动脉小动脉段。通过体外血管造影测量几何、弹性和生物力学特征。通过免疫组织化学研究O-N应激标志物。
VD缺乏组内半径减小;壁厚和壁厚/管腔直径比增加;切向壁应力和弹性模量降低。壁横截面积、内膜-中膜面积%无差异。虽然血管壁的弹性成分减少,但α-平滑肌肌动蛋白(α-SMA)免疫染色强度无变化。4-羟基-2-壬烯醛(HNE)的脂质过氧化标志物显著升高,而其他O-N应激标志物染色强度(聚(ADP)核糖、3-硝基酪氨酸)未改变。
已发生内向性肥厚重塑。这些损伤的潜在背景可能涉及氧化损伤标志物(HNE)的初始变化。这些机制可能导致VD缺乏时心血管疾病发病率增加。