Seven days after injection,Nissl staining was used toobserve the

Seven days after injection,Nissl staining was used toobserve the morphological change in hippocampal CA1 regions.Results:Intracerebroventricular injection of Aβ_(1-40)induced an increase in phosphorylatedMKK3/MKK6 and p38 MAPK expressions in hippocampal tissue.These increases,in combination with enhanced interleukin (IL)-1β protein expression and reducedphospho-MAPKAPK2 and phospho-Hsp27 expression,mediate the Aβ-inducedactivation of cell death events as assessed by cleavage of procaspase-9,-3,and -7and caspase-3 substrate PARP cleavage.Pretreatment NVP-BGJ398体外 with SF (100 mg/kg and 200mg/kg daily,3 weeks) significantly prevented Aβ_(1-40)-induced increases in phos-phorylated MKK3/MKK6 and p38 MAPK

expression.The Aβ_(1-40)-induced in-crease in IL-1β protein level was attenuated by pretreatment with SF.In addition,Aβ_(1-40)-induced decreases in phosphorylated MAPKAPK2 and Hsp27 expressionwere abrogated by administration of SF.In parallel with these findings,Aβ_(1-40)-induced changes in activation of caspase-9,caspase-7,and caspase-3 wereinhibited by pretreatment with SE Conclusion:SF prevents Aβ_(1-40)-induced neu-rotoxicity through suppression of MKK3/MKK6-p38 MAPK activity and IL-1expression and upregulation of phospho-Hsp27 expression.
目的:利用Boyden

chamber体外迁移体系以及活体状态下观察基质细胞衍生因子-1(SDF-1)对间充质干细胞(MSC)迁移的影响。方法:利用Boyden chamber体外迁移体系,先观察不同浓度hSDF-1对MSC迁移的影响,随后利用活体迁移体系,观察MSC转染Ad-hSDF-1后迁移的变化。最后利用上述体系经不同的阻断剂分别处理MSC,观察其对MSC迁移的影响。结果:MSC体外迁移能力随着hSDF-1α浓度递增而逐渐增强,并且Wortmannin、LY294002、PD98059、SB203580、PKC-ζ假底物、U70312、AMD3100、Verapamil对MSC迁移均有影响,其中PKC-ζ假底物、U73122、AMD3100对MSC迁移阻断的效应最显著。结论:SDF-1/CXCR4所介导的MSC迁移与PI3K、MAPK、PI-PLC/PKC等信号途径有关,且PKC途径可能处于中心环节。
目的研究血小板源性生长因子(PDGF)对人胚胎肺纤维细胞(HFL1)的增殖作用。方法采用四甲基偶氮唑蓝法检测不同浓度PDGF对HFL1的增殖作用,观察不同浓度细胞外信号调节激酶抑制剂PD98059、p38激酶抑制剂SB203580及PI-3K激酶抑制剂Wortmannin(WMN)对PDGF诱导HFL1增殖作用的影响。结果PDGF 并且 很少 50 ng/ml时对HFL1的诱导增殖作用明显,并呈剂量依赖性;PD98059 1μmol/L、WMN 100 nmol/L、SB2035805μmol/L可抑制PDGF诱导的HFL1增殖。结论PDGF诱导HFL1增殖是通过蛋白激酶和PI-3K信号转导途径实现的。
目的:探讨p38丝裂原活化蛋白激酶(p38mitogen-activated protein kinase,p38MAPK)信号转导对幽门螺杆菌(Heli-cobacter pylori,Hp)感染的胃上皮细胞MKN45中环氧合酶(cyclooxygenase-2,COX-2)表达的调控作用,揭示Hp感染引发胃癌的部分机制。方法:采用实时荧光定量-PCR(real-time

fluorogentic quantitative-PCR,RFQ-PCR)检测Hp标准株NCTC11637感染对MKN45细胞中COX-2 mRNA表达的影响,Western印迹法检测Hp感染MKN45细胞后p38MAPK信号通路的激活情况;运用p38MAPK特异性抑制剂SB203580阻断p38MAPK信号通路后,观察Hp对MKN45细胞COX-2 mRNA表达的影响。结果:Hp感染MKN45细胞后COX-2mRNA水平明显上调,Hp感染后3、6、9和12h时COX-2 mRNA的表达量分别为正常值的3.0、7.2、5.1和4.3倍,各时间组COX-2 mRNA表达均明显高于对照组(P<0.01)。结论:Hp感染能激活p38MAPK信号通路,通过p38MAPK信号转导上调COX-2的表达,这可能是Hp感染引发胃癌的重要机制之一。
目的探讨单核细胞趋化蛋白-1(MCP-1)诱导体外培养的肾小管上皮细胞转分化的作用及其与细胞整合素连接激酶(ILK)表达变化的关系。方法体外培养的HKC,以未处理的HKC为阴性对照,以8ng/mlTGF-β1处理的HKC为阳性对照,以不同浓度的MCP-1(0.1、1.0、10、100ng/ml)处理细胞,或以同一浓度的MCP-1(1ng/ml)在不同时间点(0h、12h、24h、36h、48h、72h)处理细胞。用半定量RT-PCR方法测定各组HKC细胞α-SMAmRNA的表达,Westernblot方法测定各组HKC细胞α-SMA及ILK表达。在上述实验基础上进一步观察MEK抑制剂(PD98059,10μmol/L),p38MAPK抑制剂(SB203580,5μmol/L)和ROCK抑制剂(Y27632,500μmol/L)对HKC细胞ILK表达的影响。结果MCP-1(0.1、1.

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