Objective To assess the role of p38 MAPK in protective effect of remifentanil preconditioning(RPC) on myocardial ischemia reperfusion injury in rat hearts.Methods Male Spargue-Dawley rats weighing 300 g to 350 g were ...Objective To assess the role of p38 MAPK in protective effect of remifentanil preconditioning(RPC) on myocardial ischemia reperfusion injury in rat hearts.Methods Male Spargue-Dawley rats weighing 300 g to 350 g were used.They were randomly assigned to 1 of 8 groups: Control(CON,saline vehicle),SB 203580(SB,a p38 MAPK inhibitor),RPC,ischemia preconditioning(IPC),SB+RPC,SB+IPC, RPC+SB and IPC+SB.Infarct size(IS),a percentage of the area at risk(AAR),was determined by triphenyltetrazolium(TTC) staining.Tissue simple were processed from the entire AAR of left ventricle for the determination of p38 MAPK protein expression(5 hearts/group).The bands representing the proteins were visualised using an enhanced chemiluminescence detection system.Results IS/AAR was reduced by IPC or RPC,compare to CON.SB administered prior to PC abolished effect of IS/AAR reduction of IPC but RPC Treatment of SB prior to sustained ischemia diminished both protective effect of RPC and IPC on IS/AAR.In IPC group,phospho-p38 MAPK protein increased significantly within 5 min ischemia and remained elevating at 30 min reperfusion,while phospho-p38 MAPK protein in RPC increased significantly at 30 min reperfusion only.Conclusion The activation of p38 MAPK acts as a mediator of RPC,while it may have trigger and mediator effects in IPC.展开更多
从Th细胞因子平衡的角度着手,探讨CpG-ODN在防治放射性肺纤维化中的作用机理。使用单次全肺照射15 Gy的雌性C57BL/6小鼠建立放射性肺损伤模型,通过酶联免疫吸附测定法连续20周检测小鼠体内Th1/Th2相关细胞因子和促纤维化细胞因子的表达...从Th细胞因子平衡的角度着手,探讨CpG-ODN在防治放射性肺纤维化中的作用机理。使用单次全肺照射15 Gy的雌性C57BL/6小鼠建立放射性肺损伤模型,通过酶联免疫吸附测定法连续20周检测小鼠体内Th1/Th2相关细胞因子和促纤维化细胞因子的表达水平,免疫组化法评估肺泡巨噬细胞、肺组织纤维化和丝裂原活化蛋白激酶(Mitogen-activated protein kinase,MAPK)家族主要蛋白的磷酸化水平。实验结果显示,CpG-ODN能促进Th1型细胞因子分泌,同时抑制Th2型细胞因子分泌,导致Th1型免疫反应占主导优势,从而抑制肺泡巨噬细胞的聚集活化,降低促纤维化细胞因子TGF-β1、IGF-1的表达,下调MAPK通路的活化。这提示CpG-ODN能通过调节电离辐射后Th1/Th2型细胞因子的失衡而抑制放射性肺纤维化的发生。展开更多
文摘Objective To assess the role of p38 MAPK in protective effect of remifentanil preconditioning(RPC) on myocardial ischemia reperfusion injury in rat hearts.Methods Male Spargue-Dawley rats weighing 300 g to 350 g were used.They were randomly assigned to 1 of 8 groups: Control(CON,saline vehicle),SB 203580(SB,a p38 MAPK inhibitor),RPC,ischemia preconditioning(IPC),SB+RPC,SB+IPC, RPC+SB and IPC+SB.Infarct size(IS),a percentage of the area at risk(AAR),was determined by triphenyltetrazolium(TTC) staining.Tissue simple were processed from the entire AAR of left ventricle for the determination of p38 MAPK protein expression(5 hearts/group).The bands representing the proteins were visualised using an enhanced chemiluminescence detection system.Results IS/AAR was reduced by IPC or RPC,compare to CON.SB administered prior to PC abolished effect of IS/AAR reduction of IPC but RPC Treatment of SB prior to sustained ischemia diminished both protective effect of RPC and IPC on IS/AAR.In IPC group,phospho-p38 MAPK protein increased significantly within 5 min ischemia and remained elevating at 30 min reperfusion,while phospho-p38 MAPK protein in RPC increased significantly at 30 min reperfusion only.Conclusion The activation of p38 MAPK acts as a mediator of RPC,while it may have trigger and mediator effects in IPC.
文摘从Th细胞因子平衡的角度着手,探讨CpG-ODN在防治放射性肺纤维化中的作用机理。使用单次全肺照射15 Gy的雌性C57BL/6小鼠建立放射性肺损伤模型,通过酶联免疫吸附测定法连续20周检测小鼠体内Th1/Th2相关细胞因子和促纤维化细胞因子的表达水平,免疫组化法评估肺泡巨噬细胞、肺组织纤维化和丝裂原活化蛋白激酶(Mitogen-activated protein kinase,MAPK)家族主要蛋白的磷酸化水平。实验结果显示,CpG-ODN能促进Th1型细胞因子分泌,同时抑制Th2型细胞因子分泌,导致Th1型免疫反应占主导优势,从而抑制肺泡巨噬细胞的聚集活化,降低促纤维化细胞因子TGF-β1、IGF-1的表达,下调MAPK通路的活化。这提示CpG-ODN能通过调节电离辐射后Th1/Th2型细胞因子的失衡而抑制放射性肺纤维化的发生。
