摘要
目的观察EPO在大鼠肺缺血再灌注后对FKN(fractalkine)及MCP-1表达的影响,探讨EPO在肺缺血再灌注损伤中的作用及相关机制。方法将72只健康的wista大鼠随机分为三组:假手术组(A)、缺血再灌注组(B)和EPO实验组(C),各组取缺血45min、再灌60min、再灌120min3个时间点,各时间点随机分8只大鼠。观察各组各时间点肺组织病理变化,并测量肺的湿干重比(W/D)及肺组织中炎性趋化因子FKN、血浆中MCP-1的含量。结果①病理变化及肺干湿重比值显示EPO对肺缺血再灌注损伤有保护作用。②EPO实验组(C)中FKN(fractalkine)、MCP-1的表达与缺血再灌注组(B)相比均有所下降,有统计学意义。结论①EPO对大鼠肺急性缺血再灌注损伤起保护作用。②该保护作用可能是通过减少炎性趋化因子FKN及MCP-1的表达来实现的。
Objective To observe the expression of FKN MCP-1 in the lung and plasma respectively and explore the possible mechanisms of EPO on lung ischemia-reperfusion injury of the rats.Methods 72 wistar rats were divided into three groups randomly：sham group（A）、ischmia-refusion group（B） and rhEPO-pretreated groups（C）.At three time spots（45min ischemia 60min and 120min reperfusion） plasma sample and the whole right lung were collected from the rats in the groups lung histopathological changes were observed lung tissue wet/dry ratio FKN and MCP-1content were determined also.Results Histopathological changes showed the lung injury were ameliorated by rhEPO pretreament.Compared with B group the content of FKN and MCP-1 were significantly reduced.Conclusion EPO can protect lung from ischemia-refusion injury.EPO attenuates ischemia-reperfusion by reducing the production of FKN and MCP-1 in the lung and plasma respectively.
出处
《当代医学》
2011年第3期37-39,共3页
Contemporary Medicine
基金
山西省科技攻关项目(20090311059-2)
山西省留学人员管理委员会科研资助项目(98)
