Antioxidant ameliorating effects against H2O2-induced cytotoxicity in primary endometrial cells

Oxidative stress and a disrupted antioxidant system are involved in a variety of pregnancy complications. In the present study, the role of vitamin E (Vit E) and folate as radical scavengers on the GSH homeostasis in stress oxidative induced in rat endometrial cells was investigated. Primary endometrial stromal cell cultures treated with 50 and 200?µM of H₂O₂ and evaluated the cytoprotective effects of Vit E (5?µM) and folate (0.01?µM) in H₂O₂-treated cells for 24?h. Following the exposure of endometrial cells to H₂O₂ alone and in the presence of Vit E and/or folate, cell survival, glutathione peroxidase (GPx) and glutathione reductase activities and the level of reduced glutathione (GSH) were measured. Cell adhesions comprise of cell attachment and spreading on collagen were determined. Flow cytometric analysis using annexin V was used to measure apoptosis. H₂O₂ treatment showed a marked decrease in cell viability, GPx and GR activities and the level of GSH. Although Vit E or folate had some protective effect, combination therapy with Vit E and folate attenuated all the changes due to H₂O₂ toxicity. An increasing number of alive cells was showed in the cells exposed to H₂O₂ (50?µM) accompanied by co-treatment with Vit E and folic acid. The present findings indicate that co-administration of Vit E and folate before and during pregnancy may maintain a viable pregnancy and contribute to its clinical efficacy for the treatment of some idiopathic infertility.     

油酰乙醇胺对人脐静脉内皮细胞血管细胞黏附分子-1表达的影响

目的探讨油酰乙醇胺(OEA)对肿瘤坏死因子α(TNF-α)诱导的人脐静脉内皮细胞血管细胞黏附分子-1(VCAM-1)表达的影响。方法体外培养人脐静脉内皮细胞,分别加入3种不同浓度的OEA(10,50,100μmol/L)或非诺贝特(10,50,100μmol/L)共同孵育10 h,再加入TNF-α共同孵育6 h,采用实时定量逆转录聚合酶链式反应和酶联免疫吸附剂检测测定VCAM-1以及mRNA和蛋白的表达,并采用Western blot方法检测过氧化物酶体增殖物激活受体α(PPAR-α)的蛋白表达。结果与非诺贝特相比,不同浓度的OEA更加显著地抑制人脐静脉内皮细胞VCAM-1mRNA和蛋白的表达,随着浓度的增大,抑制作用逐渐增强。Western bolt结果显示OAE能明显增强PPAR-α蛋白的表达。结论OEA对TNF-α引起的内皮细胞受损起到保护作用,其机理可能与上调过PPAR-α有关。     

阿托伐他汀对内皮细胞微粒诱导人脐静脉内皮细胞VCAM-1和ICAM-1表达的影响

目的:探讨阿托伐他汀对内皮细胞微粒(EMPs)诱导的人脐静脉内皮细胞(HUVECs)表达血管细胞粘附分子(VCAM)-1和细胞间粘附分子(ICAM)-1的影响。方法:取生长良好的第4,5代人脐静脉内皮细胞,将细胞分为3大组:对照组、EMPs组、EMPs+阿托伐他汀组。对照组加入培养基,EMPs组以不同浓度的EMPs(0/mL,1×102/mL,1×103/mL,1×104/mL,1×105/mL)与HUVECs共同孵育24 h,EMPs+阿托伐他汀组以不同浓度的阿托伐他汀(0.05,0.1,1.0,10μmol.L-1)与HUVECs作用1 h后,加入105/mL EMPs共同孵育24 h。分别采用实时荧光定量聚合酶链反应和蛋白免疫印迹方法检测VCAM-1和ICAM-1 mRNA和蛋白的表达。结果:HUVECs受EMPs刺激后,VCAM-1和ICAM-1 mRNA及蛋白表达呈浓度依赖性增加,阿托伐他汀可不同程度上抑制EMPs的作用。结论:阿托伐他汀抗动脉粥样硬化作用可能部分与抑制EMPs诱导的内皮细胞VCAM-1和ICAM-1的表达有关。     

丁苯酞对缺氧人脐静脉血管内皮细胞Ang-2蛋白表达的影响

目的:探讨药物丁苯酞(NBP)对人脐静脉血管内皮细胞(HUVEC)缺氧损伤的保护作用及其对血管生成素2(Ang-2)表达的影响。方法:体外培养HUVEC,建立稳定的内皮细胞缺氧损伤模型。试验分为正常对照组、缺氧损伤模型组、NBP组,按要求分别给予药物处理后,用CCK-8法检测细胞活力,采用免疫细胞化学方法和图像定量分析技术检测平均吸光度,比较各组Ang-2蛋白表达的变化;Western Blot法检测各组Ang-2蛋白的表达情况。结果:NBP可提高HUVEC的存活率;与正常组比较,缺氧组Ang-2蛋白表达量明显升高(P<0.05);与缺氧组比较,NBP组Ang-2蛋白表达进一步增高(P<0.05)。结论:NBP可以上调Ang-2蛋白的表达,对HUVEC缺氧损伤有一定的保护作用。     

Protective effects of prostaglandin E1 on human umbilical vein endothelial cell injury induced by hydrogen peroxide

Aim:

To investigate the protective effects of prostaglandin E₁ (PGE₁) against H₂O₂-induced oxidative damage on human umbilical vein endothelial cells (HUVECs).

Methods:

HUVECs were pretreated with PGE₁ (0.25, 0.50, and 1.00 μmol/L) for 24 h and exposed to H₂O₂ (200 μmol/L) for 12 h, and cell viability was measured by the MTT assay. LDH, NO, SOD, GSH-Px, MDA, ROS, and apoptotic percentage were determined. eNOS expression was measured by Western blotting and real-time PCR.

Results:

PGE₁ (0.25−1.00 μmol/L) was able to markedly restore the viability of HUVECs under oxidative stress, and scavenged intracellular reactive oxygen species induced by H₂O₂. PGE₁ also suppressed the production of lipid peroxides, such as MDA, restored the activities of endogenous antioxidants including SOD and GSH-Px, and inhibited cell apoptosis. In addition, PGE₁ significantly increased NO content, eNOS protein, and mRNA expression.

Conclusion:

PGE₁ effectively protected endothelial cells against oxidative stress induced by H₂O₂, an activity that might depend on the up-regulation of NO expression.     

脉络宁注射液对人血管内皮细胞缺氧损伤的保护作用

目的:研究脉络宁注射液对人脐静脉血管内皮细胞缺氧损伤的保护作用及其机制。方法:常规进行人血管内皮细胞(HUVECs)培养,将细胞随机分为正常对照组、缺氧组和脉络宁20 mg.L-1组。采用CCK-8法检测细胞存活率;Hochest33258荧光染料检测细胞凋亡率;RT-PCR法检测各组细胞中血管内皮生长因子(VEGF),血管生成素-2(Ang-2)mRNA表达水平。结果:脉络宁注射液可显著提高缺氧损伤细胞的存活率(P<0.05);与正常对照组比较,缺氧组细胞内VEGF和Ang-2 mRNA表达水平明显增高。与缺氧组比较,脉络宁组VEGF和Ang-2的表达进一步增强,各组间比较均有差异(P<0.05)。结论:脉络宁注射液可减轻血管内皮细胞缺氧损伤,上调缺氧血管内皮细胞中VEGF和Ang-2的表达,对血管内皮细胞缺氧损伤有一定的保护作用。     

Angiotensin II type 1 receptor blockade suppresses H2O2-induced retinal degeneration in photoreceptor cells

Exposure to reactive oxygen species (ROS) leads to the development and progression of retinal degenerative diseases. However, the exact mechanisms are not fully understood. In this article, the role of angiotensin II type 1 receptor (AT1R) signaling in H₂O₂-induced retinal damage was examined. Mouse photoreceptor-derived 661?W cells were treated with the AT1R blockers valsartan, losartan and candesartan before exposure to H₂O₂. Cell viability, intracellular ROS level, mitochondrial membrane potential (MMP), cytochrome-c level, DNA fragmentation, caspase activity and gene expression were detected. Pre-treatment of 661?W cells with AT1R blockers significantly decreased H₂O₂-mediated toxicity and reduced the ROS level. In addition, apoptosis-related biochemical indicators showed that pre-incubation of AT1R blockers would elevate the MMP, decrease the release of cytochrome-c and formation of DNA fragmentation, and inhibit activities of caspase-3 and caspase-9 in exogenous H₂O₂-treated 661?W cells. Moreover, treatment with AT1R blockers suppressed the expression of Egr1, Fosl1 and Lox12. These results suggest that AT1R signaling mediates H₂O₂-induced apoptosis, at least partially through generating the ROS and increasing the levels of proapoptotic molecules in 661?W cells. AT1R blockade may provide a new therapeutic approach for preventing oxidative stress-induced retinal neural damage.     

丙氨酰谷氨酰胺二肽对人脐静脉内皮细胞ECV304缺氧缺糖损伤的保护作用

目的观察丙氨酰谷氨酰胺二肽（丙谷二肽）对人脐静脉内皮细胞ECV304缺氧缺糖损伤的保护作用,并探讨其可能的作用机制。方法在以低氧低糖培养人脐静脉内皮细胞ECV304为细胞损伤模型的基础上,以噻唑蓝（MTT）比色法优化丙谷二肽的最佳作用浓度,显微镜观察细胞形态变化,流式细胞术检测线粒体膜电位。自动生化分析仪测定乳酸脱氢酶（LDH）活性,比色法检测谷胱甘肽（GSH）、丙二醛（MDA）的浓度,RT-PCR方法检测细胞内肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）、热休克蛋白70（HSP70）、葡萄糖调节蛋白78（GRP78）和缺氧诱导因子-1α（HIF-1α）mRNA的表达。结果丙谷二肽能够使细胞在缺氧缺糖应激下存活率增加,线粒体损伤减轻,LDH分泌降低,GSH产生增加,HSP70和HIF-1α mRNA的表达增加。结论丙谷二肽对细胞缺氧缺糖损伤有明显的保护作用,这种保护作用可能与保护线粒体、维持细胞膜结构完整、上调细胞中应激基因HSP70和HIF-1α的表达有关。     

Total flavonoids from Rosa Laevigata Michx fruit attenuates hydrogen peroxide induced injury in human umbilical vein endothelial cells

The aim of the present study was to evaluate the protective effect and possible mechanism of the total flavonoids (TFs) from Rosa Laevigata Michx fruit (RLMF) against hydrogen peroxide (H₂O₂) induced damage in human umbilical vein endothelial cells (HUVECs). The cell injury caused by H₂O₂ was protected by pretreatment with the TFs for 1 h. Compared with the model group, the TFs decreased S phase cells, suppressed nuclear morphological damage, inhibited the collapse of mitochondrial membrane potentials (ΔΨm), attenuated excessive reactive oxygen species generation, reduced glutathione depletion, impacted the mitochondrial morphology change, decreased caspase-3, -9 activities, and decreased fragmented DNA. Further mechanism investigation showed that the TFs could increase the protein expressions of Procaspase-3, Bcl-2, and decrease the expressions of Bak, Bax, Bid and p53. Generally, the TFs from RLMF is an effective natural product for the treatment of cardiovascular and cerebrovascular diseases.     

辛伐他汀对脐静脉内皮细胞金属基质蛋白酶9表达的影响

目的观察辛伐他汀对脐静脉内皮细胞（human umbilical vein endothelial cell,HUVEC）金属基质蛋白酶9（matrix metalloproteinase-9,MMP-9）表达的影响。方法采用逆转录聚合酶链反应及蛋白质免疫印迹分析检测MMP-9mRNA转录和蛋白水平表达,观察辛伐他汀不同浓度及不同孵育时间HUVECMMP-9表达的影响。结果辛伐他汀呈浓度和时间依赖性减低HU-VEC的MMP-9mRNA转录和蛋白水平的表达。结论辛伐他汀可抑制HUVE CMMP-9表达,防治动脉粥样硬化。     

Genistein alleviates H2O2-induced senescence of human umbilical vein endothelial cells via regulating the TXNIP/NLRP3 axis

ContextGenistein (Gen) has shown protective effects against ageing process.ObjectiveTo explore the role of Gen on the senescence of H₂O₂-induced human umbilical vein endothelial cells (HUVECs) and investigate the possible mechanism.Materials and methodsHUVECs were treated with different concentrations of H₂O₂ (50, 100, 200 and 400 μmol/L) for 1 h or Gen administration (20, 40, 80 and 160 μg/mL) for 24 h. Functional experiments (cell counting kit-8, β-galactosidase staining and flow cytometry) were used to detect the effect of Gen on H₂O₂-induced HUVECs. After HUVECs were transfected with TXNIP overexpression plasmids, the expression of p16, p21, thioredoxin-interacting protein (TXNIP), nucleotide-binding and oligomerization domain-like receptor 3 (NLRP3), cleaved caspase-3 and cleaved caspase-1 in HUVECs were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot.ResultsH₂O₂ (200 and 400 μmol/L) inhibited the proliferation of HUVECs. At concentrations of >50 μmol/L, H₂O₂ induced the cell cycle progression arrests in G1 phase and promoted cell senescence of HUVECs. Gen had no obvious cytotoxicity to HUVECs below 160 µg/mL. H₂O₂-induced HUVEC senescence and the expression of TXNIP and NLRP3 in HUVECs were down-regulated by Gen (40 and 80 µg/mL). Expressions of TXNIP and NLRP3 in HUVECs were up-regulated by H₂O₂ but down-regulated by Gen. Overexpressed TXNIP partially reversed the suppressive effect of Gen on H₂O₂-induced senescence and apoptosis of HUVECs. Expressions of p16, p21, TXNIP, NLRP3, cleaved caspase-3 and cleaved caspase-1 in H₂O₂-treated HUVECs were inhibited by Gen, while the inhibition as such was partially reversed by overexpressed TXNIP.Discussion and conclusionsH₂O₂-induced HUVEC senescence was alleviated by Gen via suppressing the TXNIP/NLRP3 axis, which may offer a potential therapeutic approach for improving HUVEC senescence and provide a new direction for the treatment of cardiovascular disease.     

Effects of the selective COX-2 inhibitors celecoxib and rofecoxib on human vascular cells

Rheumatoid arthritis (RA) is associated with a reduced life expectancy considered to be partly caused by cardiovascular events. A growing concern is that accelerated atherosclerosis is driven by inflammatory mechanisms similar to those responsible for RA. Therefore, selective COX-2 inhibitors, which are widely used for the symptomatic treatment of pain and inflammation in RA, may have an impact on atherosclerotic processes. Their anti-inflammatory properties might provoke anti-atherogenic effects but on the other hand, selective inhibition of anti-thrombotic prostacyclin and COX-2 independent effects might promote the risk of increased prothrombotic activity. In the current study, the effects of the presently marketed selective COX-2 inhibitors celecoxib and rofecoxib on vascular cells have been investigated. Celecoxib inhibited the proliferation of human umbilical vein endothelial cells (HUVECs) in a concentration-dependent manner. At high concentrations, it induced apoptosis and the modulation of inhibitory cell cycle proteins. In contrast rofecoxib-even at high concentrations-had no effect on cell proliferation, apoptosis or cell cycle distribution indicating that celecoxib and rofecoxib do not affect the same signal transduction pathways in endothelial cells. Both drugs did not affect apoptosis induction or cell cycle proliferation in human vascular smooth muscle cells. The observed effects on endothelial cells appear to be COX-independent since both drugs selectively inhibited COX-2-activity and the applied concentrations lay beyond the IC(50) for inhibition of prostacyclin production. Regarding endothelial apoptosis as a relevant event in the initiation and progression of atherosclerosis the present data put forward the hypothesis that the presently marketed COX-2 inhibitors have a different impact on atherosclerotic processes.     

川芎嗪对高糖诱导的人视网膜血管内皮细胞增殖的影响

目的 观察川芎嗪对高糖诱导的人视网膜血管内皮细胞（HRCECs）增殖的影响。方法 将HRCECs细胞分为对照（生理盐水）组、模型（25 mmol/L葡萄糖）组和川芎嗪低、中、高浓度（50、100、200 μmol/L）组,培养48 h后,MTT细胞毒实验检测细胞增殖变化,流式细胞技术检测细胞周期,ELISA法检测血管内皮生长因子（VEGF）表达。结果 与对照组比较,高糖对HRCECs细胞增殖、分裂（M）期比例、上清VEGF浓度均具有显著促进作用（P<0.05、0.01）;与模型组比较,低、中、高浓度川芎嗪对高糖诱导的HRCECs细胞增殖、分裂（M）期比例、上清VEGF浓度均发挥显著抑制作用（P<0.05、0.01）,且呈浓度相关性。结论 川芎嗪可能通过抑制高糖诱导的HRCECs细胞VEGF高表达,阻滞细胞周期,发挥抑制HRCECs细胞增殖的作用。     

Comparison of P25 and nanobelts on Kruppel-like factor-mediated nitric oxide pathways in human umbilical vein endothelial cells

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.     

蓬子菜总黄酮对过氧化氢损伤的人脐静脉内皮细胞的保护作用

目的:探讨蓬子菜总黄酮对人脐静脉内皮细胞(human umbilical vein endothelial cells,HU-VECs)的保护及损伤修复的作用。方法:采用台盼蓝染色法,观察不同剂量蓬子菜总黄酮(12.5～400μg.mL-1)对HUVECs生长的影响;建立过氧化氢(H2O2)诱导HUVECs氧化损伤模型,采用MTT比色法检测细胞增殖,酶联免疫分析方法检测内皮素-1(endothelin,ET-1)和降钙素基因相关肽(calcitonin generelated peptide,CGRP)的分泌水平。AO/EB双染色法观察HUVECs的凋亡。结果:与模型组比较,蓬子菜总黄酮能减轻H2O2对HUVECs增殖抑制作用,促进CGRP的分泌,降低ET-1的分泌水平,抑制HUVECs的凋亡。结论:蓬子菜总黄酮对氧化损伤的HUVECs具有保护及修复作用,其机制与调节ET-1和CGRP的分泌有关。     

岩藻黄素抗H2O2诱导WI-38细胞早衰的作用研究D*

目的：探讨岩藻黄素是否具有抑制H₂O₂引起的WI-38细胞早衰的活性。方法：WI-38细胞在添加岩藻黄素的培养基中培养一定时间后经H₂O₂处理诱导发生早衰,用MTT法检测细胞活力,SA-β-半乳糖苷酶染色法检测细胞内衰老相关的β-半乳糖苷酶活性。 结果：300 μM H₂O₂处理WI-38细胞20 min可成功建立早衰细胞模型。与空白对照组相比,H₂O₂处理组细胞活力明显降低,SA-β-半乳糖苷酶阳性细胞数明显增多。5 μM和10 μM岩藻黄素组细胞活力明显高于H₂O₂处理组,SA-β-半乳糖苷酶阳性细胞数较H₂O₂组明显减少。 结论：岩藻黄素能够抑制由H₂O₂处理引起的细胞早衰,具有一定的抗衰老作用。     

Study on the action of resistin-induced human umbilical vein endothelial cell dysfunction

The aim of this paper was to investigate the effects of resistin on human umbilical vein endothelial cells (HUVECs), and to explore its role and mechanism of action in atherosclerosis. HUVECs were incubated with recombinant human resistin (0, 50, 100 ng/mL) for 24 h. ICAM-1, VCAM-1 and reactive oxygen species (ROS) were assayed by flow cytometer. ET-1, eNOS and iNOS mRNA expression were measured by semi-quantitative RT-PCR. Incubation of HUVECs with resistin resulted in an increase in ICAM-1 expression and ET-1 mRNA expression. However, resistin had no effect on VCAM-1 expression and ROS release. eNOS and iNOS mRNA expression were not altered by resistin stimulation. Adipokine resistin exerted a direct effect in promoting HUVEC dysfunction by promoting ICAM-1 and ET-1 expression. These data suggest that adipocyte-endothelium cross-talk might play an important role in the pathogenesis of cardiovascular disease in diabetes mellitus. Translated from Journal of Sun Yat-Sen University (Medical Sciences), 2006, 27(3): 258–261 [译自: 中山大学学报 (医学科学版)]     

Geniposide inhibits high glucose-induced cell adhesion through the NF-KB signaling pathway in human umbilical vein endothelial cells

Aim:

To investigate whether geniposide, an iridoid glucoside extracted from gardenia jasminoides ellis fruits, inhibits cell adhesion to human umbilical vein endothelial cells (HUVECs) induced by high glucose and its underlying mechanisms.

Methods:

HUVECs were isolated from human umbilical cords and cultured. The adhesion of monocytes to HUVECs was determined using fluorescence-labeled monocytes. The mRNA and protein levels of vascular cell adhesion molecule-1 (VCAM-1) and endothelial selectin (E-selectin) were measured using real-time RT-PCR and ELISA. Reactive oxygen species (ROS) production was measured using a fluorescent probe. The amounts of nuclear factor-kappa B (NF-κB) and inhibitory factor of NF-κB (IκB) were determined using Western blot analysis. The translocation of NF-κB from the cytoplasm to the nucleus was determined using immunofluorescence.

Results:

Geniposide (10–20 μmol/L) inhibited high glucose (33 mmol/L)-induced adhesion of monocytes to HUVECs in a dose-dependent manner. This compound (5–40 μmol/L) also inhibited high glucose-induced expression of VCAM-1 and E-selectin at the gene and protein levels. Furthermore, geniposide (5–20 μmol/L) decreased ROS production and prevented IκB degradation in the cytoplasm and NF-κB translocation from the cytoplasm to the nucleus in HUVECs.

Conclusion:

Geniposide inhibits the adhesion of monocytes to HUVECs and the expression of CAMs induced by high glucose, suggesting that the compound may represent a new treatment for diabetic vascular injury. The mechanism underlying this inhibitory effect may be related to the inhibition of ROS overproduction and NF-κB signaling pathway activation by geniposide.     

微RNA-24对过氧化氢诱导的人脐静脉血管内皮细胞凋亡的影响及作用机制

目的探讨微RNA-24(miR-24)对H2O2诱导的人脐静脉血管内皮细胞(HUVEC)存活、迁移和凋亡的影响及作用机制。方法通过转染miR-24高表达、miR-24抑制物(anti-miR-24)及其阴性对照慢病毒质粒(miR-24 NC)构建稳转细胞,3种细胞用H2O2500μmol·L^-1处理12 h。采用四甲基偶氮唑盐(MTT)法检测细胞存活率,划痕实验检测细胞迁移率,Hoechst33258染色及流式细胞术检测细胞凋亡,实时荧光定量聚合酶链反应(qRT-PCR)检测miR-24,Bax,Bcl-2和胱天蛋白酶3 mRNA表达水平,Western印迹法和免疫细胞化学法检测Bax、Bcl-2和胱天蛋白酶3蛋白表达水平。结果与miR-24 NC组比,miR-24高表达组miR-24表达升高(P<0.05),而anti-miR-24组降低(P<0.05)。与正常对照组比,H2O2组细胞凋亡率增加(P<0.05)、细胞存活和迁移率降低(P<0.05),表明氧化损伤模型构建成功。与H2O2+miR-24 NC组比,H2O2+miR-24高表达组上述指标较H2O2+miR-24 NC组升高(P<0.05),促凋亡蛋白Bax和胱天蛋白酶3 mRNA与蛋白表达量增加,抑凋亡蛋白Bcl-2 mRNA和蛋白表达量降低(P<0.05),而H2O2+anti-miR-24组可降低细胞凋亡率、增加细胞存活和迁移率,降低Bax和胱天蛋白酶3 mRNA与蛋白表达水平,增加Bcl-2 mRNA和蛋白表达水平(P<0.05)。结论氧化应激状态下,miR-24可通过上调Bax、胱天蛋白3表达和下调Bcl-2蛋白表达,促进HUVEC凋亡和抑制其存活和迁移能力。