Essential Oil from Fructus Alpiniae Zerumbet Protects Human Umbilical Vein Endothelial Cells In Vitro from Injury Induced by High Glucose Levels by Suppressing Nuclear Transcription Factor-Kappa B Signaling.

Essential Oil from Fructus Alpiniae Zerumbet Protects Human Umbilical Vein Endothelial Cells In Vitro from Injury Induced by High Glucose Levels by Suppressing Nuclear Transcription Factor-Kappa B Signaling.
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高山姜精油通过抑制核转录因子-Kappa B 信号传导,在体外保护人脐静脉内皮细胞免受高血糖引起的损伤

DOI:
10.12659/msm.906463
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发表时间:
2017-10-04
期刊:
Medical science monitor : international medical journal of experimental and clinical research
影响因子:
--
通讯作者:
Shen X
Shen X
中科院分区:
其他
文献类型:
--
作者:
Huang N;Xu Y;Zhou H;Lin D;Zhang B;Zhang Y;Pan D;Tao L;Liu X;Shen X

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在中国,果实的精油,果果果果果(FAZ)用于治疗心血管疾病。最近的体外研究表明,FAZ(EOFAZ)的精油可以保护内皮细胞免受损伤。由于糖尿病的患病率及其对心血管系统的影响,这项研究的目的是研究eofaz对人类脐静脉内皮细胞(HUVEC)的影响的机理,在体外用高葡萄糖处理。乳酸脱氢酶(LDH)泄漏测定法用于检测HUVEC损伤。肿瘤坏死因子-Alpha(TNF-α),白介素8(IL-8)和核转录因子-KAPPA B(NF-κB)p65亚基DNA结合活性。通过蛋白质印迹研究了与NF-κB途径相关蛋白,相关蛋白,细胞间粘附分子1(ICAM-1)和血管细胞粘附分子-1(VCAM-1)的表达。使用免疫荧光评估了HUVEC中NF-κB的细胞位置。细胞活力和LDH泄漏测定法表明,Eofaz降低了葡萄糖诱导的HUVEC损伤。 Eofaz抑制了葡萄糖诱导的IL-8,TNF-α,ICAM-1和VCAM-1的分泌,NF-κB的p65亚基转移到内皮细胞核中。 Western印迹证实,Eofaz阻断了高葡萄糖水平诱导的NF-κB的激活。 Eofaz降低了高葡萄糖诱导的p65/DNA结合以抑制NF-κB激活。这项体外研究的发现表明,用eofaz对HUVEC的治疗具有保护性作用,以抵抗NF-κB信号传导途径高葡萄糖水平的影响。
In China, the essential oil of the fruit, Fructus Alpiniae zerumbet (FAZ), is used to treat cardiovascular diseases. Recent in vitro studies have shown that the essential oil of FAZ (EOFAZ) can protect endothelial cells from injury. Because of the prevalence of diabetes mellitus and its effects on the cardiovascular system, the aim of this study was to investigate the mechanism of the effects of EOFAZ on human umbilical vein endothelial cells (HUVECs) treated with high levels of glucose in vitro. The lactate dehydrogenase (LDH) leakage assay was used to detect HUVEC injury. Tumor necrosis factor-alpha (TNF-α), interleukin-8 (IL-8), and nuclear transcription factor-kappa B (NF-κB) p65 subunit DNA-binding activity was detected. The expression of NF-κB pathway-associated proteins, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) was studied by Western blotting. The cellular location of NF-κB in HUVECs was evaluated using immunofluorescence. Cell viability and LDH leakage assays showed that high glucose-induced HUVEC injury was reduced by EOFAZ. High glucose-induced secretion of IL-8, TNF-α, ICAM-1, and VCAM-1 was reduced, and translocation of the p65 subunit of NF-κB to the endothelial cell nucleus was inhibited by EOFAZ. Western blotting confirmed that EOFAZ blocked the activation of NF-κB induced by high glucose levels. EOFAZ reduced high glucose-induced p65/DNA binding to inhibit NF-κB activation. The findings of this in vitro study showed that treatment of HUVECs with EOFAZ had a protective role against the effects of high glucose levels via the NF-κB signaling pathway.
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