Suppr超能文献

牡荆素通过 Wnt/β-catenin 和 Nrf2 信号通路保护高糖诱导的内皮细胞凋亡和氧化应激。

Vitexin protects against high glucose-induced endothelial cell apoptosis and oxidative stress via Wnt/β-catenin and Nrf2 signalling pathway.

机构信息

Department of Endocrinology, Baoshan Branch, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.

Department of Endocrinology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai, People's Republic of China.

出版信息

Arch Physiol Biochem. 2024 Jun;130(3):275-284. doi: 10.1080/13813455.2022.2028845. Epub 2022 Mar 7.

Abstract

UNLABELLED

Vitexin, a polyphenolic flavonoid, has been reported to be traditionally applied in the treatment of diabetes, cancer and cardiovascular diseases.

OBJECTIVE

The aim of this study was to investigate the anti-apoptosis and anti-oxidation effect and the potential mechanism of vitexin on high glucose-induced HUVECs.

MATERIALS AND METHODS

A high dose of glucose was added to HUVECs to establish an model. The cell viability was detected by CCK8 and flow cytometry assays. 2,7-dichlorodihydrofluorescein diacetate, colorimetry, and enzyme-linked immunosorbent assay were performed to detect oxidative stress. Besides, top flash and western blotting were employed to evaluate the effect of vitexin on Wnt/β-catenin. Furthermore, a Wnt/β-catenin inhibitor (KYA1797K) was used to confirm whether Wnt/β-catenin is involved in the protection of vitexin. At the same time, RT-PCR and western blot were performed to determine the effect of vitexin on Nrf2, while immunofluorescence assays were employed for the assessment of Nrf2 localisation. Then, in order to validate that Nrf2 plays an important role in the anti-oxidant effect of vitexin, methods were utilised to silence Nrf2 gene.

RESULTS

Herein, vitexin inhibited the proliferation and apoptosis of HG-mediated HUVECs. Mechanically, vitexin disrupted Wnt/β-catenin signalling pathway, thus resulting in the decrease of apoptosis in HG-induced HUVECs. A Wnt/β-catenin inhibitor (KYA1797K), was used for reverse verification. In the meantime, vitexin administration decreased reactive oxygen species (ROS) production and malondialdehyde (MDA) content and increased superoxide dismutase (SOD) activity in HG-induced HUVECs. Further investigations have revealed vitexin activated Nrf2 in HUVEC under high glucose, which was involved in its anti-oxidant effects.

CONCLUSION

Our investigation demonstrated that vitexin protected HUVECs from high glucose-induced injury via up-regulation of Wnt/β-catenin and Nrf2 signalling pathway. These results suggested that vitexin might serve as a potential drug for atherosclerosis and cardiovascular complications of diabetes.

摘要

未加标签

牡荆素,一种多酚类黄酮,据报道传统上用于治疗糖尿病、癌症和心血管疾病。

目的

本研究旨在探讨牡荆素对高糖诱导的 HUVECs 的抗凋亡和抗氧化作用及其潜在机制。

材料和方法

向 HUVECs 中加入高剂量葡萄糖建立模型。通过 CCK8 和流式细胞术检测细胞活力。使用 2,7-二氯二氢荧光素二乙酸酯、比色法和酶联免疫吸附试验检测氧化应激。此外,还采用顶闪和 Western blot 检测牡荆素对 Wnt/β-catenin 的影响。另外,使用 Wnt/β-catenin 抑制剂(KYA1797K)来确认 Wnt/β-catenin 是否参与了牡荆素的保护作用。同时,通过 RT-PCR 和 Western blot 来确定牡荆素对 Nrf2 的影响,并用免疫荧光法来评估 Nrf2 的定位。然后,为了验证 Nrf2 在牡荆素的抗氧化作用中发挥重要作用,采用沉默 Nrf2 基因的方法。

结果

在此,牡荆素抑制了 HG 介导的 HUVECs 的增殖和凋亡。从机制上讲,牡荆素破坏了 Wnt/β-catenin 信号通路,从而导致 HG 诱导的 HUVECs 凋亡减少。使用 Wnt/β-catenin 抑制剂(KYA1797K)进行反向验证。同时,牡荆素给药降低了 HG 诱导的 HUVECs 中活性氧(ROS)的产生和丙二醛(MDA)的含量,增加了超氧化物歧化酶(SOD)的活性。进一步的研究表明,牡荆素在高糖条件下激活了 HUVEC 中的 Nrf2,这与其抗氧化作用有关。

结论

我们的研究表明,牡荆素通过上调 Wnt/β-catenin 和 Nrf2 信号通路来保护 HUVECs 免受高糖诱导的损伤。这些结果表明,牡荆素可能作为一种治疗糖尿病动脉粥样硬化和心血管并发症的潜在药物。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验