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)₂ induced 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)₂ significantly 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.

进行这项研究以调查钒化合物造成的损害，并探讨小ber碱（BBR）对人脐静脉内皮细胞（HUVEC）的保护作用。BBR是在黄连中发现的一种具有生物活性的小分子，黄连是传统中药用于治疗糖尿病的药物。BBR也已显示可降低糖尿病患者的血糖。进行MTT分析以观察双（乙酰丙酮基）-氧化钒[VO（acac）₂ ]或偏钒酸钠（NaVO ₃）和BBR对HUVEC生存力的影响。HUVEC的单层渗透性是通过测量跨内皮电阻（TER）来评估的。通过ELISA检测内皮一氧化氮合酶（eNOS）活性。进行流式细胞术以检测活性氧（ROS）的产生。结果表明，以浓度依赖性方式用50–400μM钒化合物处理可降低HUVEC的活力，而0.01–1μMBBR可有效保护HUVEC免受钒化合物对细胞活力的抑制作用。在HUVEC中，100和200μMVO（acac）₂也会诱导高渗透性并降低eNOS活性。虽然0.01–1μMBBR的渗透率没有改善，但无法逆转VO（acac）₂-诱导的eNOS活性变化，但是BBR处理增加了对照细胞中的eNOS活性。添加200μMVO（acac）_2可显着诱导HUVEC中ROS的生成，而0.01或0.1μMBBR可逆转ROS的变化。总之，BBR对钒化合物引起的HUVEC损伤具有保护作用，这不是由eNOS介导的，而是与细胞内ROS降低有关。