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首页> 外文期刊>Medical science monitor : >Angiotensin II-Induced Apoptosis of Human Umbilical Vein Endothelial Cells was Inhibited by Blueberry Anthocyanin Through Bax- and Caspase 3-Dependent Pathways
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Angiotensin II-Induced Apoptosis of Human Umbilical Vein Endothelial Cells was Inhibited by Blueberry Anthocyanin Through Bax- and Caspase 3-Dependent Pathways

机译:蓝莓花青素通过Bax和胱天蛋白酶3依赖性途径抑制血管紧张素II诱导的人脐静脉内皮细胞凋亡。

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BACKGROUND This study aimed to investigate the inhibitory effect of blueberry anthocyanin (BBA) on Angiotensin II (Ang II)-induced apoptosis of human umbilical vein endothelial cells (HUVECs), and its regulation mechanisms involving Bax and Caspase 3. MATERIAL AND METHODS HUVECs were first treated by different concentrations of Ang II (10–9, 10–8, 10–7, 10–6, 10–5, and 10–4 mol/L) and BBA (80, 40, 20, 10, 5, and 2.5 μg/ml). After 24 h and 48 h of treatment, MTT was performed to detect the viability of HUVECs. Then, HUVECs were randomly divided into the Ang II group (10–6 mol/L Ang II) and Ang II + BBA group (10–6 mol/L Ang II and 20 μg/ml BBA), and the apoptosis rate was detected by flow cytometry. Western blot analysis was performed to detect the expression of Bax and Caspase 3 in these 2 groups. During the whole process, HUVECs without any treatments served as the control group. RESULTS The cell viability of HUVECs was significantly reduced by Ang II in a time- and concentration-dependent manner ([i]P[/i]<0.05), while BBA significantly elevated the cell viability of HUVECs until a peak of 20.0 μg/ml. The apoptosis rate of HUVECs was significantly increased by Ang II ([i]P[/i]<0.01) and reduced by the BBA intervention ([i]P[/i]<0.05). Ang II significantly elevated the expression of Bax and Caspase 3 in HUVECs, but their expression was significantly inhibited by BBA. CONCLUSIONS BBA increased cell viability and reduced apoptosis rate of HUVECs induced by Ang II through Bax- and Caspase 3-dependent pathways.
机译:背景技术本研究旨在探讨蓝莓花色苷(BBA)对血管紧张素II(Ang II)诱导的人脐静脉内皮细胞(HUVECs)凋亡的抑制作用,以及其对Bax和Caspase 3的调控机制。首先用不同浓度的Ang II(10-9、10-8、10-7、10-6、10-5和10-4 mol / L)和BBA(80、40、20、10、5,和2.5μg/ ml)。治疗24小时和48小时后,进行MTT以检测HUVEC的生存力。然后,将HUVECs随机分为Ang II组(10–6 mol / L Ang II)和Ang II + BBA组(10–6 mol / L Ang II和20μg/ ml BBA),并检测其凋亡率通过流式细胞仪。进行蛋白质印迹分析以检测这两组中Bax和Caspase 3的表达。在整个过程中,未经任何治疗的HUVEC作为对照组。结果Ang II以时间和浓度依赖性的方式显着降低了HUVEC的细胞活力([i] P [/ i] <0.05),而BBA则显着提高了HUVEC的细胞活力,直至达到峰值20.0μg/毫升血管紧张素Ⅱ显着提高HUVECs的凋亡率([i] P [/ i] <0.01),而BBA干预则降低其水平([i] P [/ i] <0.05)。 Ang II显着提高HUVEC中Bax和Caspase 3的表达,但BBA显着抑制了它们的表达。结论BBA通过Bax和Caspase 3依赖性途径增加了Ang II诱导的HUVEC的细胞活力并降低了其凋亡率。

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