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排序方式: 共有243条查询结果,搜索用时 15 毫秒
1.
目的:研究中药单体组方梓葛冻干粉对人脐静脉内皮细胞(HUVECs)缺氧/复氧损伤的保护作用。方法:体外培养HUVECs,采用Krebs液建立缺氧/复氧损伤模型。用梓葛冻干粉干预后,采用MTT比色法测定细胞活力、黄嘌呤氧化酶法测定细胞内超氧化物歧化酶(SOD)活性、硫代巴比妥酸显色法测定丙二醛(MDA)含量、硝酸还原酶法测定一氧化氮(NO)含量、2,4-二硝基苯肼显色法测定细胞外乳酸脱氢酶(LDH)释放量;Western blot法分析细胞凋亡相关蛋白Bcl-2,Bax,Caspase-3的表达。结果:与模型组相比,梓葛冻干粉12.5 mg.L-1显著提高细胞活力(P<0.05);梓葛冻干粉49.0,24.5,12.5 mg.L-1均显著提高缺氧/复氧后细胞SOD活性(P<0.05);梓葛冻干粉24.5,12.5 mg.L-1能显著减少LDH的释放量及降低MDA和NO的含量(P<0.05),并上调细胞Bcl-2蛋白表达(P<0.05,P<0.01);梓葛冻干粉49.0,24.5,12.5 mg.L-1显著降低Bax的表达并上调Bcl-2/Bax(P<0.05,P<0.01),且梓葛冻干粉49.0,24.5 mg.L-1显著降低Caspase-3的表达(P<0.01)。结论:梓葛冻干粉可显著拮抗缺氧/复氧对HUVECs的损伤,可能与其抑制细胞过氧化损伤,增强细胞抗氧化和抗凋亡能力有关。 相似文献
2.
目的 探讨人脐静脉血管内皮细胞(humanumbilicalveinendothelialcells, HUVEC)在慢性髓性白血病细胞株K562细胞条件培养基作用下氧化还原状态的变化与其增殖活性间的关系,观察谷胱甘肽合成抑制剂丁胱亚磺酰亚胺(buthioninesulfoxine, BSO)在上述条件下对HUVECs的作用,为探索相应的抗肿瘤血管生成治疗策略提供新思路。方法 用K562细胞条件培养基、谷胱甘肽合成抑制剂共同或单独处理HUVEC,检测HUVEC细胞内氧化还原状态以及细胞活力的改变。结果 K562细胞条件培养基明显促进内皮细胞的增殖,并促进内皮细胞氧化型与还原型谷胱甘肽(GSSG与GSH)、辅酶Ⅱ(NADP+与NADPH)两对氧化和还原性物质同时增高,但GSSG/GSH、NADP+ /NADPH比值未变。BSO显示出对HUVEC生长的明显抑制,引起HUVEC中GSH、NADPH含量明显降低、GSSG/GSH、NADP+ /NADPH比值升高;在K562细胞条件培养基的同时作用下,BSO对HUVEC的生长抑制作用增强, 使细胞内GSSG/GSH、NADP+ /NADPH比值进一步提高。结论 慢性髓性白血病细胞条件培养基使得血管内皮细胞对BSO的生长抑制作用更加敏感,其机制与内皮细胞氧化还原状态的改变密切相关。 相似文献
3.
灵芝多糖对肿瘤细胞与内皮细胞相互作用的影响 总被引:4,自引:0,他引:4
目的研究灵芝多糖(GlPS)抗肿瘤作用及其机制。方法通过相差显微镜和间接免疫荧光的方法鉴定了人脐静脉内皮细胞(HUVECs)。采用MTT法检测GlPS对人前列腺癌细胞(PC-3M)和HUVECs增殖的影响。检测GlPS对PC-3M细胞与HUVECs粘附的影响。采用transwell双层小室观察GlPS对PC-3M迁移穿过单层HUVECs的影响。结果GlPS对PC-3M无直接细胞毒作用,对HUVECs增殖无显著性作用。GlPS能够减少粘附和迁移穿过单层内皮细胞的肿瘤细胞数目。结论灵芝多糖通过抑制肿瘤细胞粘附并迁移穿过内皮细胞发挥其抗肿瘤作用。 相似文献
4.
It was recently shown that exposure to ZnO nanoparticles (NPs) could induce endoplasmic reticulum (ER) stress both in vivo and in vitro, but the role of ER stress in ZnO NP induced toxicity remains unclear. Because macrophages are sensitive to ER stress, we hypothesized that stressing macrophages with ER stress inducer could enhance the toxicity of ZnO NPs. In this study, the effects of ER stress inducer thapsigargin (TG) on the toxicity of ZnO NPs to THP-1 macrophages were investigated. The results showed that TG enhanced ZnO NP induced cytotoxicity as revealed by water soluble tetrazolium-1 (WST-1) and neutral red uptake assays, but not lactate dehydrogenase (LDH) assay. ZnO NPs dose-dependently enhanced the accumulation of intracellular Zn ions without the induction of reactive oxygen species (ROS), and the presence of TG did not significantly affect these effects. In the co-culture, exposure of THP-1 macrophages in the upper chamber to ZnO NPs and TG significantly reduced the viability of human umbilical vein endothelial cells (HUVECs) in the lower chamber, but the release of tumor necrosis factor α (TNFα) was not induced. In summary, our data showed that stressing THP-1 macrophages with TG enhanced the cytotoxicity of ZnO NPs to macrophages and macrophage-endothelial co-cultures. 相似文献
5.
Manyu Gu Shuyi Wang Wandi Cao Dejian Yan Yi Cao 《Journal of applied toxicology : JAT》2022,42(4):651-659
Recently, we reported that titanium dioxide (TiO2) materials activated endothelial cells via Kruppel-like factor (KLF)-mediated nitric oxide (NO) dysfunction, but the roles of physical properties of materials are not clear. In this study, we prepared nanobelts from P25 particles and compared their adverse effects to human umbilical vein endothelial cells (HUVECs). TiO2 nanobelts had belt-like morphology but comparable surface areas as P25 particles. When applied to HUVECs, P25 particles or nanobelts did not induce cytotoxicity, although nanobelts were much more effective to increase intracellular Ti element concentrations compared the same amounts of P25 particles. Only nanobelts significantly induced THP-1 adhesion onto HUVECs. Consistently, nanobelts were more significant to induce the expression of intracellular adhesion molecule-1 (ICAM1) and the release of soluble ICAM-1 (sICAM-1), indicating that nanobelts were more potent to induce endothelial activation in vitro. As the mechanisms for endothelial activation, both P25 and nanobelts reduced the generation of intracellular NO as well as the expression of NO regulators KLF2 and KLF4. Combined, the results from this study indicated that the different morphologies of P25 particles and nanobelts only changed their internalization into HUVECs but showed minimal impact on KLF-mediated NO signaling pathways. 相似文献
6.
Yufang Chen Xing Du Yande Zhou Yanlin Zhang Yaping Yang Zhihua Liu Chunfeng Liu Ying Xie 《International journal of clinical and experimental pathology》2015,8(1):53-62
The aim of our study was to investigate the protective effects of Paeoniflorin (PF) against injury induced by AGE-modified bovine serum albumin (AGE-BSA) in human umbilical vein endothelial cells (HUVECs), and to examine the underlying mechanisms of these effects. A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to determine cell viability. Protein expression levels were determined by western blotting. For function-blocking experiments, we used small interfering RNA molecules (siRNA) for function-blocking experiments. At 6 h, we found that 100 μg/mL AGE-BSA reduced the viability of HUVECs. However, pretreatment with PF restored cell viability in a dose-dependent manner. AGE-BSA increased the levels of microtubule-associated protein light chain 3-II (LC3-II) and the receptor for advanced glycation end products (RAGE). Expression of p62 protein was also increased, but not at a statistically significant level. Pretreatment with PF further increased levels of LC3-II and RAGE, but reduced the expression of p62. In cells transfected with Atg5 and RAGE siRNA, cell viability and expression of LC3-II decreased in both the AGE-BSA and PF + AGE-BSA treatments. PF can protect HUVECs from AGE-BSA-induced injury by upregulating autophagy and promoting the completion of autophagy flux. RAGE plays an important role in this autophagic protection effect. 相似文献
7.
Tie-Long Chen Guang-Li Zhu Jian-An Wang Guo-Dong Zhang Hong-Fei Liu Jin-Ru Chen Yu Wang Xiao-Long He 《International journal of clinical and experimental pathology》2015,8(3):2311-2320
Little is known about the role of isorhamnetin on endothelial cell apoptosis and inflammation when insulted by TNF-α injury. In our study, HUVECs were treated with TNF-α for 6 hours. HUVECs apoptosis were detected using flow cytometry. The expressions of ICAM-1, VCAM-1, E-selectin, NF-κB, AP-1 and eNOS were determined with western blotting or flow cytometry. The results showed TNF-α increased of apoptosis and the expression of ICAM-1, VCAM-1 and E-selectin in HUVECs, accompanied by significant augmentation of NF-κB and AP-1 expression. Pretreatment with isorhamnetin significantly reduced apoptosis in TNF-α-treated HUVECs. Moreover, isorhamnetin significantly attenuated TNF-α-induced upregulation of ICAM-1, VCAM-1, AP-1, E-selectin and NF-κB expression. Meanwhile, isorhamnetin also increased the expression of eNOS. So, isorhamnetin could suppress TNF-α-induced apoptosis and inflammation by blocking NF-κB and AP-1 signaling in HUVECs, which might be one of the underlying mechanisms for treatment of coronary heart disease. 相似文献
8.
Sherif Shalaby Gautham Chitragari Brandon J. Sumpio Bauer E. Sumpio 《The International journal of angiology》2014,23(3):187-192
Extracellular signal-regulated kinase 5 (ERK5) has been reported to regulate endothelial cell integrity and protect from vascular dysfunction under continuous laminar flow. However, the effect of flow on ERK5 levels has not been determined. Confluent human umbilical vein endothelial cells (HUVECs) were seeded on fibronectin coated glass slides and serum starved for 2 hours with 1% fetal bovine serum (FBS). HUVECs were then exposed to to and fro flow (TFF), pulsatile forward flow (PFF), or continuous laminar flow (CLF) in a parallel plate flow chamber for up to 2 hours. At the end of experiment, cell lysates were prepared and immunoblotted with antibodies to total ERK5. Both CLF and TFF exhibited a decrease in ERK5 after levels after 2-hour exposure. However, the level of ERK5 for PFF remained the same. Disturbed, but not uniform pulsatile, flow decreases ERK5 levels in HUVECs. 相似文献
9.
《Pathology, research and practice》2020,216(8):153031
Oridonin has been found to be a potential anti-angiogenesis agent. However, its functional targets and the underlying mechanisms are still vague. In vitro studies we found that oridonin not only inhibited VEGF-induced cell proliferation, migration and tube formation but also caused G2/M phase arrest and triggered cellular apoptosis in HUVECs. In mechanistic studies revealed that oridonin exhibited the anti-angiogenic potency, at least in part, through the down-regulation of VEGFR2-mediated FAK/MMPs, mTOR/PI3K/Akt and ERK/p38 signaling pathways which led to reduced invasion, migration, and tube formation in HUVECs. Our results could provide evidence that oridonin exerts strong anti-angiogenesis activities via specifically targeting VEGFR2 and its signaling pathway. 相似文献
10.
Sazaly AbuBakar Meng-Hooi Shu Jefree Johari Pooi-Fong Wong 《International journal of medical sciences》2014,11(6):538-544
Alteration in the endothelium leading to increased vascular permeability contributes to plasma leakage seen in dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). An earlier study showed that senescent endothelial cells (ECs) altered the ECs permeability. Here we investigated the susceptibility of senescing human umbilical vein endothelial cells (HUVECs) to dengue virus infection and determined if dengue virus infection induces HUVECs senescence. Our results suggest that DENV type-2 (DENV-2) foci forming unit (FFU) and extracellular virus RNA copy number were reduced by at least 35% and 85% in infection of the intermediate young and early senescent HUVECs, respectively, in comparison to infection of young HUVECs. No to low infectivity was recovered from infection of late senescent HUVECs. DENV infection also increases the percentage of HUVECs expressing senescence-associated (SA)-β-gal, cells arrested at the G2/M phase or 4N DNA content stage and cells with enlarged morphology, indicative of senescing cells. Alteration of HUVECs morphology was recorded using impedance-based real-time cell analysis system following DENV-2 infection. These results suggest that senescing HUVECs do not support DENV infection and DENV infection induces HUVECs senescence. The finding highlights the possible role of induction of senescence in DENV infection of the endothelial cells. 相似文献