简介:ExposureofnaivemurineCD4^+TlymphocytestosuperantigensuchasstaphylococcalenterotoxinB(SEB)inducesastrongproliferativeresponse.ProlongedexposureorsubsequentrestimulationoftherespondingTcellpopulationwithSEBleadstotheapoptoticeventsofactivation-inducedcelldeath(AICD).ThesignalingmechanismresponsiblefortheAICDisatargetofintensiveinvestigation.However,theprecisedownstreamsignahngpathwaysofSEB-inducedAICDremainsunclear.Ourresultshereshowthatthesequentialactivationofcaspase-1/ICE-hkeandcaspase-3/CPP32-hkecysteineproteasesprobablyplaysaroleinthesignalingtransductionofSEB-inducedAICD,butcaspase-3/CPP32-hkeproteasesactivationdoesnotdependoncaspase-1-likeproteasesactivation.HerbimycinA,aspecificinhibitorofproteintyresinekinases,inhibitcaspase-3/CPP32-1ikecysteineproteasesactivation.However,itdoesnotpreventDNAfragmentationofCD4^+TcellsapoptosisinducedbySEB.TheseresultsindicatethatproteintyrosinekinasespathwayisprobablyinvolvedinthesignalingtransductionofCD4^+TcellsapoptosisinducedbySEBand“crosstalks”withthepathwayofcaspase-3/CPP32-1ikeproteasesactivation.
简介:摘要:目的 探究 IRE1信号通路在慢性阻塞性肺疾病合并肺动脉高压肺血管重构中的作用,以及法舒地尔对其的影响。方法 随机将 60只雄性 SD大鼠分为对照组、模型组、法舒地尔组。记录实验前后各组大鼠的重量,右心肥厚指数( RVHI);右心室收缩压 (RVSP);显微镜下观察大鼠肺组织的病理形态变化。结果 模型组右心室收缩压力、右心肥厚指数较对照组明显升高, p-IRE1α 、 GRP78 蛋白表达增高, 差异有统计学意义(P<0.01),法舒地尔组右心室收缩压力、右心肥厚指数较模型组降低, p-IRE1α 、 GRP78 蛋白表达降低, 差异有统计学意义(
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