Vanadium compounds induced damage of human umbilical vein endothelial cells and the protective effect of berberine
Vanadium compounds induced damage of human umbilical vein endothelial cells and the protective effect of berberine
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钒化合物对人脐静脉内皮细胞的损伤及小檗碱的保护作用
DOI：
10.1007/s10534-019-00211-6
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发表时间：
2019-10-01
期刊：
影响因子：
3.5
通讯作者：
Zhao, Ding
中科院分区：
文献类型：
--
作者：
Hou, Cong-Cong;Liang, Hong-Yu;Zhao, Ding
本研究旨在探讨钒类化合物对人脐静脉内皮细胞（HUVECs）的损伤及小檗碱（BBR）的保护作用。BBR是在黄连根茎中发现的一种具有生物活性的小分子，黄连根茎是中药治疗糖尿病的一种药物。BBR也被证明可以降低糖尿病患者的血糖。采用MTT法观察双（乙酰丙酮）-氧化钒[VO(acac)2]或元氰酸钠（NaVO3）和BBR对HUVECs活力的影响。通过测量HUVECs的跨内皮电阻（TER）来评估HUVECs的单层通透性。ELISA法检测内皮型一氧化氮合酶（eNOS）活性。流式细胞术检测活性氧（ROS）的生成。结果表明，在50 ~ 400 μM的钒浓度下，HUVECs的细胞活力呈浓度依赖性下降，而0.01 ~ 1 μM的BBR能有效保护HUVECs免受钒对细胞活力的抑制作用。100 μM和200 μM VO(acac)2诱导huvec高通透性和eNOS活性降低。而0.01-1 μM BBR没有改善细胞的通透性，也不能逆转VO(acac)2诱导的eNOS活性变化，但BBR处理使对照细胞的eNOS活性增加。200 μM VO(acac)2显著诱导HUVECs中ROS的生成，而0.01和0.1 μM BBR则逆转了ROS的变化。综上所述，BBR对钒化合物诱导的HUVECs损伤具有保护作用，这种损伤不是由eNOS介导的，而是与细胞内ROS的减少有关。
This study was conducted to investigate the damage caused by vanadium compounds and to explore the protective effects of berberine (BBR) in human umbilical vein endothelial cells (HUVECs). BBR is a biologically active small molecule found in Coptis rhizome, a remedy used in traditional Chinese medicine to treat diabetes. BBR has also been shown to lower blood glucose in diabetic patients. MTT assay was performed to observe the influence of bis(acetylacetonato)-oxidovanadium [VO(acac)2] or sodium metavanadate (NaVO3) and BBR on viability of HUVECs. The monolayer permeability of the HUVECs was assessed by measuring the transendothelial electrical resistance (TER). The endothelial nitric oxide synthase (eNOS) activity was detected by ELISA. Flow cytometry was performed to detect the generation of reactive oxygen species (ROS). The results showed that the viability of HUVECs was decreased by treatment with vanadium compounds 50–400 μM in a concentration-dependent manner, while 0.01–1 μM BBR effectively protected HUVECs from the inhibitory effects of vanadium compounds on cell viability. Also 100 and 200 μM VO(acac)2induced high permeability and decreased eNOS activity in HUVECs. While 0.01–1 μM BBR showed no improvement in the permeability, and failed to reverse the VO(acac)2-induced changes of eNOS activity, but BBR treatment increased the eNOS activity in control cells. The addition of 200 μM VO(acac)2significantly induced ROS generation in HUVECs, while 0.01 or 0.1 μM BBR reversed the change of ROS. In summary, BBR has protective effects in HUVECs damage induced by vanadium compounds, which is not mediated by eNOS, but related to reduced intracellular ROS.