甲基苯丙胺对小鼠空间学习记忆能力的影响

目的：研究甲基苯丙胺（MA）对小鼠空间学习能力的影响.方法：本研究以C57BL/6雄性小鼠为研究对象,随机分为四组：2mg·kg-1MA剂量组、5mg·kg-1 MA剂量组、10mg·kg-1 MA剂量组、及盐水对照组（Saline.。腹腔注射给药（i.p）,重复给药7天后第二天采用Morris水迷宫实验方法观察各组小鼠的空间学习能力,并进一步采用Western Blot实验方法观测了10mg·kg-1MA剂量组大脑前额叶皮质内MAPK通路ERK分子的表达情况.各组数据以均数±标准差（x±sd）表示,采用SPSS13.0统计软件,逃避潜伏期（escape latency,EL）采用重复测量方差分析,其余采用单因素方差分析（one way anova）,α取0.05.结果：10mg·kg-1MA组小鼠EL延长且大脑前额叶皮质内ERK、pERK表达降低（p〈0.05）;结论：短期内反复大剂量使用MA（10mg·kg-1）对小鼠空间学习能力有损伤,并且此损伤作用可能与MA所致小鼠前额叶皮质内ERK、pERK表达降低有关.     

和营安心方对过氧化氢损伤大鼠胚胎心肌细胞的保护作用

目的：探讨和营安心方对过氧化氢（hydrogen peroxide,H2O2）所致大鼠胚胎心肌细胞损伤的保护作用。方法：建立H2O2致大鼠胚胎心肌细胞氧化应激损伤模型,设正常对照组（Control）、过氧化氢（200μmol·L-1）模型组（Model）、和营安心方（500、250、125 mg·kg-1）三个剂量组,四甲基偶氮唑盐（3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl tetrazolium bromide,MTT）代谢率检测心肌细胞细胞活性,测定细胞培养液中乳酸脱氢酶（lactate dehydrogenase,LDH）及丙二醛（malondialdehyde,MDA）的含量。结果：H2O2组细胞活性显著性降低（P<0.01）, LDH及MDA含量显著性升高（P<0.01）;和营安心方可显著提高H2O2损伤心肌细胞的活性,减少MDA 含量（P<0.05）,降低LDH 活性（P<0.05）。结论：和营安心方对H2O2损伤的心肌细胞具有明显的保护作用,其机制可能与抑制脂质过氧化有关。     

次乌头碱配伍甘草次酸对缺氧缺糖损伤H9c2心肌细胞的保护作用及其分子机制（英文）

目的:探讨次乌头碱(HA)配伍甘草次酸(GA)对缺氧缺糖(OGD)损伤H9c2心肌细胞的保护作用及其作用机制。创新点:首次在OGD模型中证明HA+GA对H9c2心肌细胞有明显的保护作用。此作用与减少细胞坏死和凋亡有关系,且其作用机制与磷脂酰肌醇-3-激酶/蛋白质丝氨酸-苏氨酸激酶(PI3K/Akt)信号通路有关。方法:采用H9c2心肌细胞为研究对象,将其分为七组:正常组、OGD模型组、OGD+HA组、OGD+GA组、OGD+HA+GA组、OGD+LY294002组、OGD+HA+GA+LY294002组。采用Hoechst 33342染色荧光显微镜及透射电镜观察前五组的H9c2心肌细胞的形态学改变;采用酶联免疫吸附测定法(ELISA)检测前五组细胞上清液中乳酸脱氢酶(LDH)、肌酸激酶同工酶(CK-MB)以及天门冬氨酸氨基转移酶(AST)的释放量的改变;采用异硫氰酸荧光素-磷脂结合蛋白V/碘化丙啶(FITC-AV/PI)双染色法检测前五组细胞凋亡率的情况;采用蛋白质免疫印迹法(Western blot)检测加入抑制剂LY294002前后丝苏氨酸蛋白激酶(Akt)、磷酸化丝苏氨酸蛋白激酶(p-Akt)、B细胞淋巴瘤/白血病-2相关x蛋白(Bax)、B细胞淋巴瘤/白血病-2(Bcl-2)及半胱氨酸天冬氨酸蛋白酶-9(caspase-9)等细胞作用信号通路PI3K/Akt相关蛋白的情况。结论:(1)Hoechst 33342染色荧光显微镜显示OGD+HA+GA组抗凋亡作用最明显;(2)透射电镜观察OGD+HA+GA组凋亡现象改善最多;(3)LDH、CK-MB及AST的含量变化显示OGD+HA+GA组心肌细胞损伤指标降低最多(P0.05);(4)Western blot法检测结果显示HA+GA可以减少OGD对H9c2心肌细胞的损伤,其作用机制与PI3K/Akt信号通路有关。     

康脑液对脑缺血再灌注损伤大鼠血管内皮生长因子、脑源性神经生长因子、基质金属蛋白酶表达的影响

目的：通过康脑液干预观察其对脑缺血再灌注损伤大鼠血管内皮生长因子（vascular endothelial growth factor,VEGF）、脑源性神经生长因子（brain derived neurotrophic factor,BDNF）、基质金属蛋白酶（matrix metalloproteinase-9,MMP-9）表达的影响,探讨康脑液对脑缺血再灌注损伤的保护机制.方法：将雄性SD大鼠随机分为假手术组、脑缺血再灌注模型组及康脑液28.6、14.3、7.15 g·kg-1·d-1剂量组（灌胃给药7 d）,改进Longa等线栓法制备大鼠右侧大脑中动脉阻塞（middle cerebral artery occlusion,MCAO）再灌注模型.于缺血2h后再灌注（分别于再灌注后6h、12h、24 h、72 h、7d处死大鼠）;采用TTC染色法观察大鼠的脑梗死面积;免疫组织化学法观察大鼠脑组织VEGF、BDNF、MMP-9的表达.结果：比较各组缺血再灌注24 h大鼠脑梗死灶面积,发现28.6、14.3 g·kg--1·d-1剂量组较脑缺血再灌注模型组明显减小（P＜0.05）;与脑缺血再灌注模型组相比,28.6、14.3 g·kg--1·d-1剂量组各时间点的VEGF、BDNF表达量明显上调（P＜0.01）,MMP-9表达的阳性细胞明显减少（P＜0.01）,差异有统计学意义.结论：康脑液可促进大鼠局灶性脑缺血后脑组织中VEGF,BDNF的表达,同时抑制脑内MMP-9的表达,缩小脑梗死面积,发挥对神经血管单元（neurovascular unit,NVU）的保护作用,减轻脑缺血再灌注损伤.     

新型组蛋白去乙酰化酶抑制剂DWP0016诱导神经胶质瘤细胞U251周期阻滞及凋亡作用研究

目的:观察新型组蛋白去乙酰化酶( Histone Deacetylases,HDACs)抑制剂DWP0016对神经胶质瘤U251细胞株的作用,探讨诱导U251细胞周期阻滞及凋亡作用的机制.方法:采用噻唑蓝(MTT)法检测DWP0016对U251细胞株的增殖抑制作用;采用流式细胞术观察DWP0016对U251细胞周期的影响及凋亡诱导作用;采用实时定量PCR(real-time PCR)检测抑癌因子P21,P53的mRNA水平变化;蛋白免疫印迹法(Western blotting)测定Ac-H3,P21,P53,Pi3K,p-Pi3K,Akt,p-Akt的蛋白表达并进行光密度定量.结果:DWP0016抑制U251细胞增殖的半数抑制浓度(IC50=0.531 μmol·L-1)明显低于阳性对照奥沙利铂(IC50=4.792 μmol·L-1),组蛋白H3乙酰化水平显著上升;DWP0016作用后,U251细胞中细胞周期阻滞于G1期并产生凋亡,P21,P53的mRNA水平和蛋白水平明显上升,Pi3K/Akt通路中的Pi3K,Akt的磷酸化水平下降.结论:DWP0016能明显抑制U251细胞增殖,诱导细胞周期阻滞和凋亡产生,其机制与促进抑癌因子P21,P53的转录及蛋白表达,抑制细胞中Pi3K/Akt生长信号通路有关,具有良好的抗神经胶质瘤潜力和开发应用前景.     

山茶花提取物预处理对脑缺血再灌注损伤的保护作用

目的：探讨山茶花提取物（extractofCamelliajaponicaL．ECJ）预处理对小鼠脑缺血再灌注损伤的保护作用及其机制。方法：采用大脑中动脉线栓法制作小鼠大脑中动脉闭塞（MCAO）模型,观察ECJ预处理对小鼠大脑中动脉栓塞再灌注后脑梗死体积、血清小鼠神经特异性烯醇化酶（NSE）的活性及丙二醛（MDA）含量的变化。结果：与模型组对比,ECJ（15mgrkg^-1,30mg．kg^-1,60mg．kg-1）预处理明显减少脑梗塞体积,并可显著降低血清中NSE和MDA含量。结论：山茶花提取物预处理对小鼠脑缺血再灌注损伤具有明显的保护作用。     

ELABELA衍生肽ELA13通过抑制Smad和ERK信号通路减轻肾纤维化（英文）

肾脏纤维化是各种慢性肾脏疾病发展为终末期肾病的关键过程。目前尚无针对肾纤维化的特异性治疗方法。ELA13（氨基酸序列：RRCMPLHSRVPFP）是ELABELA在所有脊椎动物中的保守片段,目前对其生物学活性的研究却很少。本研究评估了ELA13对转化生长因子β1(TGF-β1)处理的NRK-52E细胞和单侧输尿管闭塞（UUO）小鼠的作用效果。首先,体外实验表明在TGF-β1诱导的NRK-52E细胞中,ELA13可以降低纤维化标志物I型胶原（CollagenI）、纤连蛋白（fibronectin）和α-平滑肌肌动蛋白（α-SMA）的表达水平。随后,在UUO诱导的小鼠肾纤维化模型中,我们发现ELA13可以通过降低血清中肌酐和尿素氮的含量来改善肾功能,并通过Masson染色、免疫组织化学、实时定量聚合酶链式反应（RT-PCR）和蛋白质印迹（westernblot）的结果证实纤维化标志物和炎症标志物的表达降低了。进一步机制研究发现,ELA13处理可抑制Smad和细胞外调节蛋白激酶（ERK）信号通路。综上所述,ELA13通过抑制Smad和ERK信号通路发挥抗肾纤维化的作用,有望成为抗肾纤维化治疗...     

PI3K/Akt信号通路部分参与了右美托咪定对异丙酚诱导的胎鼠海马神经元凋亡的保护作用（英文）

目的:研究PI3K/Akt信号通路是否参与了右美托咪定对异丙酚诱导的胎鼠海马神经元凋亡的保护作用,并初步探讨可能的作用机制。创新点:首次利用胎鼠海马神经元研究发现右美托咪定对异丙酚诱导的神经元凋亡作用部分是由PI3K/Akt信号通路介导的。方法:首先分离胎鼠海马神经元并鉴定。使用MTT法检测异丙酚对神经元活性的影响。然后将神经元分为不同的组,分别用0.1、1、10和100μmol/L右美托咪定预处理细胞,然后加入100μmol/L的异丙酚继续培养,同时设异丙酚组和正常对照组。使用蛋白质印迹(Western blot)方法检测Akt、p-Akt、Bad、p-Bad和Bcl-x L的表达变化。在100μmol/L右美托咪定预处理前加入LY294002,进一步研究PI3K/Akt途径是否参与了右美托咪定对异丙酚诱导的胎鼠海马神经元凋亡的保护作用。结论:实验结果显示,异丙酚明显降低了神经元的细胞活性及p-Akt和p-Bad的表达水平,增加了Bad的表达,从而Bcl-x L/Bad的比率升高。100μmol/L右美托咪定预处理可以逆转这种效果。LY294002可以抑制右美托咪定的保护作用,说明右美托咪定对异丙酚诱导的胎鼠海马神经元凋亡的保护作用部分是由PI3K/Akt信号通路介导的。     

AST对甲基苯丙胺诱导的PC-12细胞氧化损伤的保护作用

目的：研究AST （astaxanthin,AST）对甲基苯丙胺（methamphetamine,MA）诱导的大鼠肾上腺嗜铬细胞瘤（PC-12）细胞氧化损伤的保护作用.方法：选取PC-12细胞体外培养后,随机分为正常对照组、甲基苯丙胺组、低剂量AST（0.1 μmol·L-1）＋甲基苯丙胺组、中剂量AST （1.0 μmol·L-1）＋甲基苯丙胺组、高剂量AST（10.0 μmol·L-1）＋甲基苯丙胺组,通过研究PC-12细胞的存活率以及超氧化物歧化酶（superoxide dismutase,SOD）活性,还原性谷胱甘肽（glutathione,GSH）含量和丙二醛（malondialdehyde,MDA）含量的变化,评价AST的保护作用.结果：甲基苯丙胺能导致细胞存活率下降,同时也使SOD活性和GSH的含量降低,MDA含量增加.经过一定浓度的AST共处理后,细胞存活率显著提高,SOD活性和GSH含量也显著提高,MDA含量显著降低.结论：AST对甲基苯丙胺诱导的PC-12细胞损伤具有一定的保护作用,其机制可能与其抗氧化作用有关.     

原花青素联用胡椒碱减轻抑郁样行为的机制研究

目的：探讨原花青素（proanthocyanidin,OPC）不同剂量联用胡椒碱（piperine,PIP）的抗抑郁样行为及其机制.方法：采用慢性不可预知性温和应激模型,连续造模联合给药21d后,d 22测定小鼠悬尾、强迫游泳不动时间;用高效液相电化学法测定小鼠海马和前额叶皮层中单胺递质及其代谢产物的含量,荧光分光光度法检测全脑单胺氧化酶活性.结果：与正常组相比,模型组小鼠悬尾和强迫游泳测试中的不动时间显著增加;同时其海马、前额叶皮层中5-羟色胺（5-hydroxytryptamine,5-HT）、去甲肾上腺素（norepinephrine,NE）含量显著下降,但5-羟吲哚乙酸（5-hydroxyindoleacetic acid,5-HIAA）与5-HT比值（5-HIAA/5-HT）显著上升.OPC （50、25、12.5 mg·kg-1）剂量组联用PIP（5 mg·kg-1）能够逆转这种现象.此外,OPC （50、25、12.5 mg·kg-1）剂量组联用胡椒碱（5 mg·kg-1）组还能降低由于应激引起的单胺氧化酶（monoamine oxidase,MAO）A型活性升高,但不影响单胺氧化酶B型活性.结论：原花青素联用胡椒碱可以改善由于慢性应激对小鼠造成的抑郁样行为,其机制可能与降低单胺氧化酶活性,增加单胺递质含量有关.     

丹参水溶性有效成分对血管内皮细胞损伤保护作用的均匀设计-高通量筛选研究

目的：通过丹参七种水溶性有效成分多水平均匀设计配伍的血管内皮细胞保护作用筛选研究,评价中药有效成分的均匀设计-高通量筛选技术（uniform design-high throughput screening,UD-HTS）的应用.方法：选取原儿茶醛、原儿茶酸、咖啡酸、丹参素钠、迷迭香酸、丹酚酸A、丹酚酸B七种丹参水溶性单体有效成分七个水平（1×10-4～1×10-10 mol·L-1）进行均匀设计配伍组合,通过H2O2诱导的氧化应激损伤血管内皮细胞模型、血管内皮细胞营养剥夺模型评价各种有效成分配伍组合对药效的影响.结果：经过初筛和复筛,初步得到了2个最佳配伍组合样品（A2、B4）,其细胞存活率分别为（70±4）％,（76±3）％.不同的细胞损伤模型筛选出不同的最优配比.结论：均匀设计配伍与中药复方配伍有相似之处,均匀设计-高通量筛选技术是适用于传统多因素多水平组合特点的大规模药效筛选研究新方法.     

Protective mechanisms of hypaconitine and glycyrrhetinic acid compatibility in oxygen and glucose deprivation injury

This study investigated the protective effect of the compatibility of hypaconitine (HA) and glycyrrhetinic acid (GA) on H9c2 cells under oxygen and glucose deprivation (OGD)-induced injury, and the possible mechanisms. We found that HA+GA significantly improved pathology and morphology of the nucleus and ultrastructure of H9c2 cells under OGD as determined by Hoechst 33342 staining and transmission electron microscopy (TEM) tests. It also reduced the releases of lactate dehydrogenase (LDH), creatine kinase-myocardial band isoenzyme (CK-MB), and aspartate transaminase (AST) from the cultured supernatant of H9c2 cells, which were tested by enzyme-linked immune sorbent assay (ELISA) kits. In addition, it lessened the apoptotic rate as determined by a fluorescein isothiocyanate-annexin V/propidium iodide (FITC-AV/PI) double staining assay. It was also found that HA+GA might regulate the protein expression associated with the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway. Overall, the study demonstrated that HA+GA protected H9c2 cells against OGD-induced injury, and the signaling mechanism might be related to the PI3K/Akt signaling pathway.     

Angiopoietin-1 preconditioning enhances survival and functional recovery of mesenchymal stem cell transplantation

Objective

Mesenchymal stem cell (MSC) transplantation is a promising therapy for ischemic heart diseases. However, poor cell survival after transplantation greatly limits the therapeutic efficacy of MSCs. The purpose of this study was to investigate the protective effect of angiopoietin-1 (Ang1) preconditioning on MSC survival and subsequent heart function improvement after transplantation.

Methods

MSCs were cultured with or without 50 ng/ml Ang1 in complete medium for 24 h prior to experiments on cell survival and transplantation. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Hoechst staining were applied to evaluate MSC survival after serum deprivation in vitro, while cell survival in vivo was detected by terminal deoxynucleotidyl transferase biotin-dUPT nick end labeling (TUNEL) assay 24 and 72 h after transplantation. Heart function and infarct size were measured four weeks later by small animal echocardiography and Masson??s trichrome staining, respectively.

Results

Ang1 preconditioning induced Akt phosphorylation and increased expression of Bcl-2 and the ratio of Bcl-2/Bax. In comparison with non-preconditioned MSCs, Ang1-preconditioned cell survival was significantly increased while the apoptotic rate decreased in vitro. However, the PI3K/Akt pathway inhibitor, LY294002, abrogated the protective effect of Ang1 preconditioning. After transplantation, the Ang1-preconditioned-MSC group showed a lower death rate, smaller infarct size, and better heart functional recovery compared to the non-preconditioned-MSC group.

Conclusions

Ang1 preconditioning enhances MSC survival, contributing to further improvement of heart function.     

Heat shock protein 90 protects rat mesenchymal stem cells against hypoxia and serum deprivation-induced apoptosis via the PI3K/Akt and ERK1/2 pathways

Mesenchymal stem cell(MSC)transplantation has shown a therapeutic potential to repair the ischemic and infracted myocardium,but the effects are limited by the apoptosis and loss of donor cells in host cardiac microenvironment.The aim of this study is to explore the cytoprotection of heat shock protein 90(Hsp90)against hypoxia and serum deprivation-induced apoptosis and the possible mechanisms in rat MSCs.Cell viability was determined by3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT)assay.Apoptosis was assessed by Hoechst 33258nuclear staining and flow cytometric analysis with annexin V/PI staining.The gene expression of Toll-like receptor-4(TLR-4)and V-erb-b2 erythroblastic leukemia viral oncogene homolog 2(ErbB2)was detected by real-time polymerase chain reaction(PCR).The protein levels of cleaved caspase-3,Bcl-2,Bcl-xL,Bax,total-ERK,phospho-ERK,totaI-Akt,phospho-Akt,and Hsp90 were detected by Western blot.The production of nitric oxide was measured by spectrophotometric assay.Hsp90 improves MSC viability and protects MSCs against apoptosis induced by serum deprivation and hypoxia.The protective role of Hsp90 not only elevates Bcl-2/Bax and Bcl-xL/Bax expression and attenuates cleaved caspase-3 expression via down-regulating membrane TLR-4 and ErbB2 receptors and then activating their downstream PI3K/Akt and ERK1/2 pathways,but also enhances the paracrine effect of MSCs.These findings demonstrated a novel and effective treatment strategy against MSC apoptosis in cell transplantation.     

Neuroprotection of dexmedetomidine against propofol-induced neuroapoptosis partly mediated by PI3K/Akt pathway in hippocampal neurons of fetal rat

The aim was to investigate how the PI3K/Akt pathway is involved in the protection of dexmedetomidine against propofol. The hippocampal neurons from fetal rats were separated and cultured in a neurobasal medium. Cell viability was assayed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Then neurons were pretreated with different concentrations of dexmedetomidine before 100 μmol/L propofol was added. Akt, phospho-Akt (p-Akt), Bad, phospho-Bad (p-Bad), and Bcl-xL were detected by Western blot. Also, neurons were pretreated with dexmedetomidine alone or given the inhibitor LY294002 before dexmedetomidine pretreatment, and then propofol was added for 3 h. The results demonstrated that propofol decreased the cell viability and the expression of p-Akt and p-Bad proteins, increased the level of Bad, and reduced the ratio of Bcl-xL/Bad. Dexmedetomidine pretreatment could reverse these effects. The enhancement of p-Akt and p-Bad induced by dexmedetomidine was prevented by LY294002. These results showed that dexmedetomidine potently protected the developing neuron and this protection may be partly mediated by the PI3K/Akt pathway.     

A novel thioredoxin reductase inhibitor inhibits cell growth and induces apoptosis in HL-60 and K562 cells

Human thioredoxin reductase (TrxR) system is associated with cancer cell growth and anti-apoptosis process. Effects of 1,2-[bis(1,2-benzisoselenazolone-3(2H)-ketone)]ethane (BBSKE), a novel TrxR inhibitor, were investigated on human leukemia cell lines HL-60 and K562. BBSKE treatment induced cell growth inhibition and apoptosis in both cell lines. Apoptosis induced by BBSKE is through Bcl-2/Bax and caspase-3 pathways. Ehrlich's ascites carcinoma-bearing mice were used to investigate the anti-tumor effect of BBSKE in vivo. Tumor-bearing mice treated with BBSKE showed an increase of life span with a comparable effect to cyclophosphamide (CTX). These results suggest a potential usage of BBSKE as a therapeutic agent against non-solid tumors.     

Down-regulation of eIF5A-2 prevents epithelial-mesenchymal transition in non-small-cell lung cancer cells

Background

Epithelial-mesenchymal transition (EMT) is believed to be the critical process in malignant tumor invasion and metastases, and has a great influence on improving the survival rate in non-small-cell lung cancer (NSCLC) patients. Recent studies suggested that eukaryotic initiation factor 5A-2 (eIF5A-2) might serve as an adverse prognostic marker of survival. We detected eIF5A-2 in NSCLC A549 cells, and found that the invasive capability correlates with the eIF5A-2 expression.

Methods

Transforming growth factor (TGF)-β1 was used to induce EMT in A549 cells. Western blotting, immunofluorescence, wound healing assay, and transwell-matrigel invasion chambers were used to identify phenotype changes. Western blotting was also used to observe changes of the expression of eIF5A-2. We down-regulated the eIF5A-2 expression using an eIF5A-2 siRNA and identified the phenotype changes by western blotting and immunofluorescence. We tested the change of migration and invasion capabilities of A549 cells by the wound healing assay and transwell-matrigel invasion chambers.

Results

After stimulating with TGF-β1, almost all A549 cells changed to the mesenchymal phenotype and acquired more migration and invasion capabilities. These cells also had higher eIF5A-2 protein expression. Down-regulation of eIF5A-2 expression with eIF5A-2 siRNA transfection could change the cells from mesenchymal to epithelial phenotype and decrease tumor cell migration and invasive capabilities significantly.

Conclusions

The expression of eIF5A-2 was up-regulated following EMT phenotype changes in A549 cells, which correlated with enhanced tumor invasion and metastatic capabilities. Furthermore, in the A549 cell line, the process of EMT phenotype change could be reversed by eIF5A-2 siRNA, with a consequent weakening of both invasive and metastatic capabilities.     

Silencing of DsbA-L gene impairs the PPARγ agonist function of improving insulin resistance in a high-glucose cell model

Disulfide-bond A oxidoreductase-like protein (DsbA-L) is a molecular chaperone involved in the multimerization of adiponectin. Recent studies have found that DsbA-L is related to metabolic diseases including gestational diabetes mellitus (GDM), and can be regulated by peroxisome proliferator-activated receptor γ (PPARγ) agonists; the specific mechanism, however, is uncertain. Furthermore, the relationship between DsbA-L and the novel adipokine chemerin is also unclear. This article aims to investigate the role of DsbA-L in the improvement of insulin resistance by PPARγ agonists in trophoblast cells cultured by the high-glucose simulation of GDM placenta. Immunohistochemistry and western blot were used to detect differences between GDM patients and normal pregnant women in DsbA-L expression in the adipose tissue. The western blot technique was performed to verify the relationship between PPARγ agonists and DsbA-L, and to explore changes in key molecules of the insulin signaling pathway, as well as the effect of chemerin on DsbA-L. Results showed that DsbA-L was significantly downregulated in the adipose tissue of GDM patients. Both PPARγ agonists and chemerin could upregulate the level of DsbA-L. Silencing DsbA-L affected the function of rosiglitazone to promote the phosphatidylinositol 3-kinase (PI3K)-protein kinase B (PKB)/AKT pathway. Therefore, it is plausible to speculate that DsbA-L is essential in the environment of PPARγ agonists for raising insulin sensitivity. Overall, we further clarified the mechanism by which PPARγ agonists improve insulin resistance.     

砷剂对肿瘤多药耐药细胞株作用机理的研究

三氧化二砷（As2O3）是人们观念中的剧毒物砒霜中的有效成分．它既是一种致癌剂又有一定有益的生物学作用．本实验研究证实，砷剂在非细胞毒性剂量下能降低化疗药物阿霉素（ADM）对多耐药（multi drug resistance，MDR）肿瘤细胞株K562/ADM细胞的IC50（细胞抑制率达50％时化疗药物的浓度），表明三氧化二砷具有逆转人红白血病细胞株K562/ADM细胞MDR作用．     

甘草多糖对小鼠细胞免疫的影响

目的：观察甘草的有效成分甘草多糖（GlycyrrhizaPolysaccharide）对细胞免疫的调节作用;方法：给胃灌甘草多糖14d,测定二硝基氟苯诱导的小鼠迟发性超敏反应（DTH）,用放射免疫法检测血中IL-2、TNF—α含量,观察甘草多糖对小鼠细胞免疫功能的影响;结果：与空白组比较,甘草多糖对DTH反应有-定的增强作用,能升高血中IL-2、TNF-α含量;结论：甘草多糖能明显增强小鼠细胞免疫功能。