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Quercetin protects human brain microvascular endothelial cells from fibrillarβ-amyloid_(1–40)-induced toxicity

Acta Pharmaceutica Sinica B 2015年第1期5卷 47-54页

作者： Yongjie Li Sibai Zhou Jinze Li Yuhua Sun Hamlati Hasimu Rui Liu Tiantai Zhang Institute of Materia Medica Chinese Academy of Medical Sciences and Peking Union Medical College Xinjiang Key Laboratory of Xinjiang Uygur Medicine Xinjiang Institute of Materia Medica

Amyloid beta-peptides(Aβ) are known to undergo active transport across the blood-brain barrier, and cerebral amyloid angiopathy has been shown to be a prominent feature in the majority of Alzheimer's disease. Quercetin is a natural flavonoid molecule and has been demonstrated to have potent neuroprotective effects, but its protective effect on endothelial cells under Aβ-damaged condition is unclear. In the present study, the protective effects of quercetin on brain microvascular endothelial cells injured by fibrillar Aβ_(1–40)(f Aβ_(1–40)) were observed. The results show that f Aβ_(1–40)-induced cytotoxicity in human brain microvascular endothelial cells(h BMECs) can be relieved by quercetin treatment. Quercetin increases cell viability, reduces the release of lactate dehydrogenase, and relieves nuclear condensation.Quercetin also alleviates intracellular reactive oxygen species generation and increases superoxide dismutase activity. Moreover, it strengthens the barrier integrity through the preservation of the transendothelial electrical resistance value, the relief of aggravated permeability, and the increase of characteristic enzyme levels after being exposed to f Aβ_(1–40). In conclusion, quercetin protects h BMECs from f Aβ_(1–40)-induced toxicity.

关键词： Alzheimer’s disease Fibrillar Aβ1–40 human brain microvascular endothelial cells Quercetin

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Edaravone protected human brain microvascular endothelial cells from methylglyoxal-induced injury by inhibiting AGEs/RAGE/oxidative stress

Edaravone protected human brain microvascular endothelial ce...

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中国神经科学学会第十届全国学术会议

作者： Wenlu LI Haibin DAI Department of Pharmacy Second Affiliated HospitalZhejiang University School of Medicine

Subjects with diabetes experience an increased risk of cerebrovascular disease and stroke compared with nondiabetic age-matched individuals.Increased formation of reactive physiological dicarbonyl compound methylglyoxal（MGO） seems to be implicated in the development of diabetic vascular complication due to its protein glycation and oxidative stress effect.Edaravone,a novel radical scavenger,has been reported to display the advantageous effects on ischemic stroke both in animals and clinical trials,however,little is known about whether edaravone has protective effects on diabetic cerebrovascular injury.Using cultured human brain microvascular endothelial cells（HBMEC）,protective effects of edaravone on MGO and MGO enhancing oxygen-glucose deprivation（OGD） induced injury were investigated.Cell injury was measured by3-（4,5-dimefhylthiazol-2-yl）-2,5-diphenyltetrazolium bromide（MTT） formation,cell account,lactate dehydrogenase（LDH） release and rhodamine 123 staining.Advanced glycation end-products（AGEs） formation and receptor for advanced glycation end-products（RAGE） expression were measured by western blotting.Cellular oxidative stress was measured by reactive oxygen species（ROS） release.Treatment of MGO for 24 h significantly induced HBMEC injury,which was inhibited by pretreatment of edaravone from 10- 100 μmol/l.What’s more,treatment of MGO enhanced AGEs accumulation,RAGE expression and ROS release in the cultured HBMEC,which were inhibited by 100 μmol/l edaravone.Finally,treatment of MGO for 24 h and then followed by 3 h OGD significantly enhanced cell injury when compared with OGD only,which was also protected by 100 μmol/l edaravone.Thus,edaravone protected HBMEC from MGO and MGO enhancing OGD-induced injury by inhibiting AGEs/RAGE/oxidative stress.

关键词： edaravone human brain microvascular endothelial cells methylglyoxal advanced glycation end-products receptor for advanced glycation end-products reactive oxygen species oxygen-glucose deprivation

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β-Estradiol 17-acetate enhances the in vitro vitality of endothelial cells isolated from the brain of patients subjected to neurosurgery

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Neural Regeneration Research 2023年第2期18卷 389-395页

作者： Sonia Guzzo Pasquale De Bonis Barbara Pavan Luciano Fadiga Department of Neuroscience and Rehabilitation Section of PhysiologyUniversity of FerraraFerraraItaly Center for Translational Neurophysiology of Speech and Communication(CTNSC) Italian Institute of Technology(IIT)FerraraItaly Department of Translational Medicine and for Romagna University of FerraraFerraraItaly

In the current landscape of endothelial cell isolation for building in vitro models of the blood-brain barrier,our work moves towards reproducing the features of the neurovascular unit to achieve glial compliance through an innovative biomimetic coating technology for brain chronic implants.We hypothesized that the autologous origin of human brain mic rovascular endothelial cells(hBMECs)is the first requirement for the suitable coating to prevent the glial inflammato ry response trigge red by foreign neuroprosthetics.Therefo re,this study established a new procedure to preserve the in vitro viability of hBMECs isolated from gray and white matter specimens taken from neurosurge ry patients.Culturing adult hBMECs is generally considered a challenging task due to the difficult survival ex vivo and progressive reduction in proliferation of these cells.The addition of 10 nMβ-estradiol 17-acetate to the hBMEC culture medium was found to be an essential and discriminating factor promoting adhesion and proliferation both after isolation and thawing,suppo rting the well-known protective role played by estrogens on microvessels.In particular,β-estradiol 17-acetate was critical for both freshly isolated and thawed female-derived hBMECs,while it was not necessary for freshly isolated male-derived hBMECs;however,it did countera ct the decay in the viability of the latter after thawing.The tumo r-free hBMECs were thus cultured for up to 2 months and their growth efficiency was assessed befo re and after two periods of cryopreservation.Des pite the thermal stress,the hBMECs remained viable and suitable for re-freezing and storage for several months.This approach increasing in vitro viability of hBMECs opens new perspectives for the use of cryopreserved autologous hBMECs as biomimetic therapeutic tools,offering the potential to avoid additional surgical sampling for each patient.

关键词： β-estradiol 17-acetate 17β-estradiol cryopreservation gender-specific gray matter human brain microvascular endothelial cells surgical resections vascular protection white matter

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维普期刊数据库

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Piperlongumine Inhibits Zika Virus Replication In vitro and Promotes Up-Regulation of HO-1 Expression, Suggesting An Implication of Oxidative Stress

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Virologica Sinica 2021年第3期36卷 510-520页

作者： Weizhi Lu Linjuan Shi Jing Gao Huimin Zhu Ying Hua Jintai Cai Xianbo Wu Chengsong Wan Wei Zhao Bao Zhang Biosafety Level-3 Lab School of Public HealthSouthern Medical UniversityGuangzhou 510515China Department of Epidemiology School of Public HealthSouthern Medical UniversityGuangzhou 510515China

Owing to the widespread distribution of mosquitoes capable of transmitting Zika virus, lack of clinical vaccines and treatments, and poor immunity of populations to new infectious diseases, Zika virus has become a global public health concern. Recent studies have found that Zika virus can continuously infect human brain microvascular endothelial cells.These cells are the primary components of the blood–brain barrier of the cerebral cortex, and further infection of brain tissue may cause severe damage such as encephalitis and fetal pituitary disease. The present study found that a biologically active base, piperlongumine(PL), inhibited Zika virus replication in human brain microvascular endothelial cells, Vero cells, and human umbilical vein endothelial cells. PL also significantly increased heme oxygenase-1(HO-1) gene expression, while silencing HO-1 expression and using the reactive oxygen species scavenger, N-acetylcysteine, attenuated the inhibitory effect of PL on Zika virus replication. These results suggest that PL induces oxidative stress in cells by increasing reactive oxygen species. This, in turn, induces an increase in HO-1 expression, thereby inhibiting Zika virus replication. These findings provide novel clues for drug research on the prevention and treatment of Zika virus.

关键词： Piperlongumine Heme oxygenase-1(HO-1) Reactive oxygen species Zika virus(ZIKV) human brain microvascular endothelial cells

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