Minocycline protects the apoptosis of PC12 cells induced by 1-methyl-4-phenylpyridinium

Objective： To explore the protective effect of minocycline on the apoptosis of cellular parkinsonism models induced by MPP^＋ . Methods： Using PC12 cells as the apoptotic model of dopaminergic neurons, MC and MPP^＋ were added into the culture medium of PC12 cells, and using MTr to assay the cell viability and metabolic state; The cells apoptosis was assayed by electrophoresis method and using flow cytometry FACS to assay the apoptosis ratio. Results： Added the MPP^＋ to get the concentration of 10μmol/L, the cellular parkinsonism model of apoptosis had been prepared. The pre-treatment of MC （ 100/μmol/L） could significantly increase the PC12 cell viability. The apoptosis ratio of MC＋MPP^＋ group was significantly lower than that of MPP^＋ group, but was still significantly higher than that of control group. Conclusion： MC may protect the cell apoptosis induced by MPP^＋ to some extent.     

Role of Endoplasmic Reticulum Stress in Silica-induced Apoptosis in RAW264.7 Cells

Objective We investigated the role of endoplasmic reticulum stress(ERS) in silica-induced apoptosis in alveolar macrophages in vitro. Methods RAW264.7 cells were incubated with 200 μg/mL silica for different time periods. Cell viability was assayed by the MTT assay. Cell apoptosis was evaluated by DAPI staining, flow cytometry analysis, and Western blot analysis of caspase-3. Morphological changes in the endoplasmic reticulum were observed by transmission electron microscopy. The expression of ERS markers binding protein(BiP) and CCAAT-enhancer-binding protein homologous protein(CHOP) was examined by Western blotting and real-time PCR. As an inhibitor of ERS, 4-phenylbutyric acid(4-PBA) was used in the experiments. Results Silica exposure induced nuclear condensation and caspase-3 expression in RAW264.7 cells. The number of apoptotic cells increased after silica exposure in a time-dependent manner. Silica treatment induced expansion of the endoplasmic reticulum. In addition, the expression of BiP and CHOP increased in silica-stimulated cells. Furthermore, 4-PBA treatment inhibited silica-induced endoplasmic reticulum expansion and the expression of Bi P and CHOP. Moreover, 4-PBA treatment attenuated nuclear condensation, reduced apoptotic cells, and downregulated caspase-3 expression in silica-stimulated cells. Conclusion Silica-induced ERS is involved in the apoptosis of alveolar macrophages.     

Set up Alzheimer＇s Disease Cell Apoptosis Model with PC-12 Cell Induced by Aβ25-35

Objective: To prepare an apoptosis cell model of Alzheimer Disease ( AD ) by PC-12 cells treated with β-amyloid protein (Aβ). Methods: PC-12 cells were incubated with differ-ent concentrations of Aβ25-35 for different duration in vitro. The cell viability was detected by MTT as-say. Morphological features of apoptosis were analyzed with Hoechst 33258/Prorlidium iodide dual staining, The level of intracellular free calcium ([Ca^2 ]i) was calculated by Fura-2 / AM fluorescence ratio imaging. Results: ① The viability of PC-12 cells was significantly decreased in prolrrrtion to concentration of Aβ25-35 and duration of exposure to Aβ25-35. ②The apoplotic cells appeared in a time and concentration-dependent manner, and the maximal apoptosis happened at 48 h after execute to 20μmol/ L of Aβ25-35 and 36 h to 30μmol/ L. Cell death reached the peak at 12-24 h later than the apoptotic peak. ③([Ca^2 ]i) of PC-12 cells was increased in prolrrrtion to duration of exposure to the same concentration of Aβ25-35. The time of the highest increase rate of [Ca^2 ]i was about 12 h earlier than that of apoptosis. Conclusion : An AD cell model using the PC-12 cells induced with Aβ25-35 displays aseries of chanqes related to apoptosis, which may be related to elevation of [Ca^2 ]i.     

Effects of olfactory ensheathing cells on hydrogen peroxide- induced apoptosis in cultured dorsal root ganglion neurons

Background Olfactory ensheathing cells （OECs） can promote many kinds of neuron growth and axonal extension. The aim of the study was to investigate the effects of co-culturing with OECs on neuron apoptosis in vitro. Methods Apoptosis was induced by treatment of cultured dorsal root ganglion neurons with 1 mmol/L hydrogen peroxide （H2O2）. Cells were randomly arranged into the following treatment groups. In group 1, OECs at different density （10^4/ml to 8×10^5/ml） were added immediately after H2O2 treatment and cells were co-cultured for 24 hours. In group 2, OECs were added at different time points （0, 4, 8, 12 and 24 hours） after H2O2 treatment. Apoptotic cell death was determined by Hoechst 33258 staining and flow cytometry （FCM）. Cell viability was determined by using methyl thiazoleterazolium （MTT） assays. Results The results showed in the Hoechest 33258 staining, FCM and MTT that OECs have both the density-dependent protection and time-dependent protection on neuron apoptosis. The apoptosis decreased and the dorsal root ganglion neuron viability increased, when the density of OECs was increased in co-culture groups. But further increasing OEC density above 2×10^5/ml （i.e. 8×10^5/ml） failed to exert additional protection. As the interval between adding H2O2 and adding OECs was increased, the amounts of apoptosis cells were also increased. When OECs were added 24 hours after H2O2, no significant protection was observed. Conclusion These results indicated that OECs could protect dorsal root ganglion neurons from apoptosis induced by H2O2 in a density- and time-dependent manner.     

Inhibition of microvascular endothelial cell apoptosis by angiopoietin-1 and the involvement of cytochrome C

Background Angiopoietin-1 （Ang-1） is an endothelial-specific growth factor that can promote angiogenesis. Studies demonstrated that Ang-1 can inhibit apoptosis of umbilical endothelial cells, but so far little is known about its effects on apoptosis of microvascular endothelial cells. With the apoptotic model of murine- cerebral-derived microvascular endothelial cells （bEnd.3） induced by serum-free culture,we attempted to clarify the molecular mechanism of bEnd.3 apoptosis, particularly its relation to cytochrome C （Cyt C）. Methods The cultured microvascular endothelial cell strain, bEnd.3 cell, was employed. An apoptotic model of bEnd.3 was established by serum-free culture. Flow cytometry after Annexin labeling and PI staining were used to assess the apoptotic effects of Ang-1 on bEnd.3, and the expression of Bax/Bcl-2, caspase 8, caspase 3, and Cyt C were detected with Western blotting and ELISA. Results The apoptotic rate of bEnd.3 cells after stimulation with Ang-1 （100 ng/L） in serum-free medium was significantly higher than that in control group. Ang-1 inhibited early-stage apoptosis more than late-stage apoptosis provided by propidium iodide （PI） and AnnexinV double staining. The inhibition of Ang-1 on bEnd.3 cell apoptosis was strengthened with the increase in concentration （0-400 ng/ml）. Ang-1 could decrease the expression of Bax, caspase3 and 8, and increase that of Bcl-2. The results of ELISA indicated that Ang-1 significantly decreased CytC content in cytoplasm and increase that in mitochondria. Conclusions Ang-1 could inhibit bEnd.3 apoptosis induced by serum-free medium culture. The apoptosis was associated with decreased Bax expression, increased Bcl-2 expression, which result in Cyt C transferring from mitochondria to cytoplasm, and then caspases activation are reduced and cell apoptosis is suppressed.     

Roles of Protein Kinase C and Fructose in Hepatic Injury Caused by Obstructive Jaundice

Summary： The regulating mechanism in hepatic injury caused by obstructive jaundice （OJ） was examined in this study. Rat hepatocytes were harvested by in situ collagenase perfusion and subjected to primary culture. The heptocytes were pre-treated with various concentrations of protein kinase C （PKC） agonist PMA and its inhibitor chelerythrine and cultured for 20 min. After the treatment, 50μmol/L glycochenodeoxycholate （GCDC） was added and the cells were cultured for an additional 24 h. Cells were then detected by flow cytometry （FCM） and TUNEL. After hepatocytes were treated with different concentrations of fructose and 100μM GCDC, the cells were examined by FCM and TUNEL. Experimental obstructive jaundice （BDL） was induced by double ligation of the bile duct. After BDL, the rats were fed with or without fructos and sacrificed 3, 7, 14 and 21 days after the ligation. The apoptotic status was observed in liver of all rats with TUNEL and PKC protein in liver of OJ was studied by immunohistochemical method. Our results showed that PMA increased GCDC-induced apoptosis and chelerythrine decreased GCSX-induced apoptosis in a concentration-dependent manner. After the treatment with fructose of different concentrations, 100μM GCDC decreased the apoptotic rate and the apoptotic rate decreased with the increase of fructose concentration. The apoptotic rate of liver was related to the time of OJ. Without the treatment of fructose, PKC and apoptosis index （AI） were highest 14 days after the bile duct ligation. With the treatment of fructose, apoptosis index （AI） and PKC were decreased from the 14th day after the bile duct ligation. It is concluded that PKC is involved in the regulation of apoptosis in the liver cells with OJ and plays important roles in the development and progression of liver injury caused by OJ. Fructose can protect hepatocytes in the bile salt-induced apoptosis by regulating PKC.     

Dracorhodin perchlorate suppresses proliferation and induces apoptosis in human prostate cancer cell line PC-3

The growth inhibition and pro-apoptosis effects of dracorhodin perchlorate on human prostate cancer PC-3 cell line were examined. After administration of 10-80 μmol/L dracorhodin perchlorate for 12-48 h, cell viability of PC-3 cells was measured by MTT colorimetry. Cell proliferation ability was detected by colony formation assay. Cellular apoptosis was inspected by acridine orange-ethidium bromide fluorescent staining, Hoechst 33258 fluorescent staining, and flow cytometry (FCM) with annexin Ⅴ-FITC/propidium iodide dual staining. The results showed that dracorhodin perchlorate inhibited the growth of PC-3 in a dose- and time-dependent manner. IC50 of dracorhodin perchlorate on PC-3 cells at 24 h was 40.18 μmol/L. Cell clone formation rate was decreased by 86% after treatment with 20 μmol/L of dracorhodin perchlorate. Some cells presented the characteristic apoptotic changes. The cellular apoptotic rates induced by 10-40 μmol/L dracorhodin perchlorate for 24 h were 8.43% to 47.71% respectively. It was concluded that dracorhodin perchlorate significantly inhibited the growth of PC-3 cells by suppressing proliferation and inducing apoptosis of the cells.     

Damaging effect of cigarette smoke extract on primary cultured human umbilical vein endothelial cells and its mechanism

Objective To investigate the cellular effects of cigarette smoke extract (CSE) on primarily cultured human umbilical vein endothelial cells (HUVEC). Methods The effects of CSE (5%-20%) and nicotine (10^4 mol/L) on HUVEC viability, proliferation, angiogenesis and apoptosis were observed. Results CSE decreased HUVEC survival rate and angiogenesis after 24 h as well as its proliferation after 48 h in a dose-dependent manner. Moreover, CSE induced apoptosis of HUVEC as indicated in condensation of nuclear chromatin and the presence of hypodiploid DNA. HUVEC incubated with CSE for 24 h gave a significant decrease in the expression of Bcl-2 as well as the decline in the Bcl-2/Bax ratio accompanied with the loss of mitochondrial membrane potential and excess cytosolic calcium. Our study also observed that p53 protein level decreased, rather than increased in cells treated with CSE. Nicotine had no discernible inhibitory effects on the above indices of HUVEC. Conclusion Exposure to CSE other than nicotine causes inhibition of viability,proliferation and differentiation of HUVEC. CSE-induced HUVEC injury is mediated in part through accelerated apoptosis but independent of p53 pathway. It appears that mitochondria have played a key role in the apoptosis of HUVEC induced by CSE.     

TGF-β_1和TL1A在高糖所致血管内皮细胞凋亡中的作用

目的:观察高糖条件下,内皮细胞分泌的TGF-β1和TL1A对细胞凋亡的影响。方法:以22.4mmol/L葡萄糖培养细胞不同时间(0h,6h,12h,24h,48h),RT-PCR和Westernblot检测内皮细胞TGF-β1和TL1A表达,Annexin V-FITC/PI双染色、流式细胞仪测定细胞凋亡率。结果:高糖条件下HUVECTGF-β1和TL1A表达增加(均P<0.01),22.4mmol/L葡萄糖培养条件下,TGF-β1的表达高峰在12h,TL1A高表达峰值在48h。高糖条件下细胞凋亡率明显增加(21.06%±3.05%vs3.09%±0.32%,P<0.01)。在正常糖培养的HUVEC中加入外源性的TGF-β1和TL1A,均导致细胞凋亡率显著增高(15.26%±2.93%,55.70%±8.91%vs3.09%±0.32%,均P<0.01),在高糖培养液中加入抗TL1A抗体能明显抑制细胞凋亡发生(4.28%±0.48%vs21.06%±3.05,P<0.01),但加入抗TGF-β1抗体却不能逆转高糖诱导的细胞凋亡(20.93%±3.21vs21.06%±3.05%,P>0.05)。结论:高糖上调内皮细胞TGF-β1和TL1A的表达,TL1A介导高糖引起内皮细胞凋亡的作用,高糖引起内皮细胞凋亡与TGF-β1无关。     

丹参复合微乳抗垂体后叶素致大鼠急性心肌缺血的药效学研究

目的探讨丹参复合微乳(Co-ME)抗垂体后叶素致大鼠急性心肌缺血的药效。方法采用舌下静脉注射垂体后叶素造成心肌缺血的方法,检测丹参复合微乳和空白微乳、丹参酮微乳、丹酚酸微乳、丹参酮混悬液各给药组在注射垂体后叶素30min后血清中磷酸肌酸激酶(PCK)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)活性和丙二醛(MDA)的含量。结果丹参复合微乳、丹参酮微乳、丹酚酸微乳和丹参酮混悬液均可在一定程度上改善注射垂体后叶素诱导的急性心肌缺血,减少PCK、LDH活性及MDA的生成量、提高心肌组织SOD活性,且以丹参复合微乳疗效最为显著,具有优于丹参酮微乳、丹酚酸微乳的作用趋势,并优于丹参酮混悬液。结论微乳载药体系可明显促进丹参酮的吸收,提高生物利用度,对急性心肌缺血具有治疗作用,丹参酮和丹酚酸复合可增加疗效。     

丹参多酚酸对大鼠缺血心肌线粒体酶的影响

目的:探讨丹参多酚酸对大鼠心肌缺血再灌注过程中线粒体Na+,K+-ATP酶和Ca2+-ATP酶的影响。方法:采用健康Wistar大鼠(n=40)建立Langendorff离体心脏灌注模型,并分为4组。对照组用Krebs液持续灌注120 min;缺血再灌注组平衡30 min后全心缺血30 min,再灌注60 min;丹参多酚酸预处理组平衡5 min后加入丹参多酚酸使其在灌流液中终浓度为14μmol/L,持续灌注25 min后全心缺血30 min,再灌注60 min;丹参多酚酸后处理组平衡30 min后全心缺血30 min,加入丹参多酚酸使其在灌流液中终浓度为14μmol/L,再灌注60 min。TTC染色观察心肌梗死面积,并用心肌梗死面积、乳酸脱氢酶(LDH)活性和心脏血流动力学(包括心率、主动脉流量、冠状动脉流量和心输出量)的变化评估大鼠心肌的损伤程度。利用差速离心法提取线粒体,并通过紫外分光光度法测定心肌线粒体Na+,K+-ATP酶和Ca2+-ATP酶的活性。结果:丹参多酚酸预处理组的心肌梗死面积和LDH活性均显著低于缺血再灌注组([24.47±2.14)%比(34.30±2.31)%、(81.46±13.39)U/g比(142.6±6.46)U/g,均P<0.05],缺血再灌注组与后处理组无明显差异。丹参多酚酸对缺血再灌注心肌的血液动力学没有明显作用,只是冠脉流量有较小幅度的增加。丹参多酚酸预处理组线粒体Na+,K+-ATP酶和Ca2+-ATP酶活性显著高于缺血再灌注组([6.12±0.42)U/mg比(4.29±0.28)U/mg、(3.42±0.16)U/mg比(2.62±0.96)U/mg,均P<0.05],而与对照组无明显差异。丹参多酚酸后处理组线粒体Na+,K+-ATP酶和Ca2+-ATP酶活性与缺血再灌注组无统计学差异。结论:丹参多酚酸可以维持心肌线粒体Na+,K+-ATP酶和Ca2+-ATP酶的活性,通过降低缺血再灌注对心肌线粒体的损伤保护心肌。     

丁苯酞对Aβ25-35诱导的阿尔茨海默病细胞模型的保护作用

目的 研究丁苯酞对Aβ25-35诱导的AD细胞模型的保护作用及其作用机制.方法 取对数生长期的N2a细胞,用20 μmol/LAβ25-35建立阿尔茨海默病细胞模型;实验分为AD组、丁苯酞组和对照组,其中丁苯酞组设立4个药物浓度梯度的亚组,分别为0.1、1、10、100μmol/L丁苯酞.MTT法检测细胞存活率;流式细胞仪检测细胞凋亡率;倒置相差显微镜下观察细胞形态学变化;qRT-PCR检测细胞TNF-β和IL-1β的mRNA含量.结果 与对照组比较:AD组细胞存活率显著下降,细胞凋亡率明显增加,贴壁细胞数量明显减少,突起结构减少,TNF-α和 IL-1β mRNA表达增高(P＜0.05);与AD组比较:丁苯酞组的细胞存活率提高,细胞凋亡率下降,贴壁细胞数量增多且结构较正常,TNF-α和IL-1β的mRNA表达减少(P＜0.05).结论 丁苯酞对Aβ25-35诱导的AD细胞模型具有保护作用,可能与抑制TNF-α和IL-1β等炎性因子的表达有关.     

同型半胱氨酸致动脉粥样硬化的机制研究

目的通过观察不同浓度同型半胱氨酸(Homocysteine,Hcy)干预对人脐静脉血管内皮细胞(HumanUmbilical Vein Endothelial Cells,HUVEC)和氧化应激的影响,探讨其在动脉粥样硬化(Atherosclerosis,AS)中的作用。方法体外培养HUVEC,将其分为正常对照组(Hcy 0μmol·L-1)、Hcy干预组(浓度分别为50、100、200、500μmol·L-1)、100μM Hcy+叶酸+VitB12治疗组,每个浓度组再分为24、48、72h三个时间组。MTT法检测各组细胞增殖抑制率,测定各浓度Hcy干预HUVEC 72h的氧化应激损伤指标。结果各浓度Hcy干预组随着Hcy浓度增高及干预时间延长HUVEC的细胞增殖抑制率增加,500μM Hcy 72h干预组最明显(P<0.05)。HUVEC内H2O2和MDA含量随Hcy浓度的增加而增加,Hcy100～500μM组与对照组比较差异均有统计学意义(P<0.01);Hcy100～500μM组HUVEC内SOD活性和T-AOC活性均较对照组降低(P<0.01),并且Hcy的浓度越高降低程度越明显。100μM Hcy+叶酸+VitB12治疗组与对照组比较上述各指标的差异均无统计学意义(P>0.05)。结论 Hcy抑制HUVEC增殖的作用呈剂量依赖关系,病理水平Hcy可以增强氧化应激损伤反应,而叶酸和VitB12对Hcy所致氧化应激损伤有一定的拮抗作用。     

晚期糖基化终产物修饰人血清白蛋白对人血管内皮细胞的生长抑制作用

目的　探讨晚期糖基化终产物 (AGE)在糖尿病难愈创面形成和发展中的作用机制。方法　将人脐静脉内皮细胞株ECV30 4细胞与不同浓度的AGE修饰人血清白蛋白 (AGE HSA)在体外共同培养。应用四甲基偶氮唑蓝 (MTT)比色法、锥虫蓝排斥实验和活细胞计数检测AGE HSA对血管内皮细胞的生长抑制作用。采用AnnexinVFitc和碘化丙啶 (PI)染色 ,通过流式细胞仪检测细胞凋亡百分率 ,同时应用荧光共聚焦显微镜观察凋亡或死亡细胞AnnexinVFitc和PI的荧光染色 ;利用透射电镜和光镜观察AGE HSA对内皮细胞的形态学影响。结果　内皮细胞经 12 .5、2 5和 5 0 μg/mlAGE HSA干预 2d后 ,各干预组细胞数与对照组比较无明显差异 (均P >0 0 5 ) ,而于 4d和 6d后明显低于对照组 ,细胞增殖抑制率显著上升。内皮细胞经 10 0或 2 0 0 μg/mlAGE HSA干预 6、12、2 4、4 8h后 ,MTT法测其吸光度A值在各时相点均显著低于对照组 (P <0 0 1) ,同时内皮细胞出现特异性的凋亡形态学变化 ,AnnexinVFitc阳性和 /或PI阳性的细胞逐渐增多 ,流式细胞仪测定的各时相点凋亡细胞百分率均显著高于对照组 (P <0 0 1) ,且凋亡或死亡细胞数量随AGE HSA作用时间及浓度的增加而增多。结论　AGE HSA能抑制内皮细胞增殖 ,并可以诱导其凋亡 ,而且与作用时间及浓     

花色苷类植物化学物抑制血管内皮细胞氧化应激损伤作用的结构-效应关系研究

目的 对膳食中常见的21种花色苷抑制血管内皮细胞氧化应激损伤作用进行结构-效应关系研究,探索与花色苷内皮保护作用密切相关的结构特征,筛选出作用较显著的化合物单体.方法 不同浓度氧化低密度脂蛋白(ox-LDL,50、100、150、200μg/ml)处理内皮细胞24 h,MTT法检测细胞活力,确定IC_(50);以不同浓度(50、100、200μmol/L)的花色苷预处理内皮细胞2 h后,100μg/ml的ox-LDL继续处理细胞24 h,MTT法检测各组细胞活力;100 μmoL/L花色苷预处理内皮细胞2 h后,100μg/ml ox-LDL继续处理细胞24 h,按试剂盒说明书测定细胞培养上清液MDA和NO水平;根据各组细胞活力、MDA和NO值,结合不同花色苷的结构特征进行结构.效应关系分析.结果 ox-LDL能明显抑制内皮细胞活力,并呈浓度依赖关系,IC_(50)为100μg/ml.不同花色苷对内皮细胞活力、MDA生成和NO释放的影响存在显著相关性.花色苷对内皮细胞氧化应激损伤的抑制作用与其总-OH数量及B环-OH数量呈明显正相关;B环3',4'-邻苯二羟基和C环3-OH能增强花色苷的抑制作用,而甲基化和糖苷化能明显削弱其作用;A环6-OH可能削弱其抑制作用,B环5'和A环5位-OH对其作用无显著影响;葡萄糖取代与半乳糖取代对花色苷抑制作用的影响无显著差异,而单糖取代较之双糖取代能明显增强其抑制作用.Delphinidin和Delphinidin-3-glucoside分别是2种作用最显著的花色苷元和花色苷.结论 B环3',4'-邻苯二羟基和C环3-OH是花色苷抑制内皮细胞氧化损伤的重要结构特征.     

TL1A抗体通过抑制活性氧产生阻止高糖诱导血管内皮细胞凋亡

目的:探讨TL1A抗体在高糖所致活性氧(ROS)增多及细胞凋亡中的作用。方法:将培养的人脐静脉内皮细胞分为正常对照组、正常糖+TL1A组、高糖对照组、高糖+SOD+CAT组、高糖+TL1A抗体组和高渗对照组。采用流式细胞术检测人脐静脉内皮细胞ROS生成量;Annexin V/PI荧光双染色,流式细胞仪检测细胞凋亡率。结果:与正常对照组相比,高糖对照组ROS生成量增加53%,细胞凋亡率达正常的5.8倍(P<0.01)。于正常糖培养液中加入外源性TL1A蛋白,活性氧的生成量及细胞凋亡率均明显增多,显著高于正常对照组和高糖对照组(P<0.01);在高糖培养液中加入9μg/ml TL1A抗体,活性氧生成量由(71.63±6.61)降至(50.63±4.05),细胞凋亡率由(23.70±3.20)%降至(5.07±0.47)%(P<0.01)。结论:TL1A抗体通过抑制ROS产生阻止高糖诱导血管内皮细胞凋亡。     

热休克蛋白A12B降低脂多糖诱导的血管内皮细胞通透性

目的 探讨脂多糖诱导下血管内皮细胞热休克蛋白A12B(HSPA12B)表达的改变及其对血管内皮通透性的影响.方法 体外传代培养人脐静脉内皮细胞,并将其分为空白组(未进行任何处理)、脂多糖(1 μg/mL)诱导组、脂多糖+HSPA12B高表达组(转染HSPA12B过表达质粒)和脂多糖+阴性质粒对照组(转染阴性对照质粒).采用电阻抗检测仪检测脐静脉内皮细胞的跨内皮电阻抗,流式细胞仪检测血管内皮钙黏素(VE-cadherin)的表达,蛋白质印迹、PCR检测HSPA12B的表达改变.结果 脐静脉内皮细胞经脂多糖诱导后,细胞中HSPA12B表达在0～12 h内上调,12 h时达高峰.HSPA12B能使脐静脉内皮细胞的跨内皮电阻抗值明显升高(P＜0.001),并能完全对抗脂多糖诱导造成的跨内皮电阻抗值的下降(P＜0.001).HSPA12B能使脐静脉内皮细胞细胞膜上VE-cadherin的表达上调.结论 HSPA12B可能通过上调VE-cadherin表达降低血管内皮细胞的通透性,从而保护血管内皮的屏障功能.