05);抑制组p38MAPK活性在各时相点的变化无显著性差异(P>0.05),除离体前及再灌注120 min两组肝脏的p38MAPK活性无显著性差异外,其余各时相点p38MAPK活性均显著性低于对照组(P0.05);至再灌注60 min及120 min,对照组ICAM1 所以 mRNA的表达水平显著性高于组内其它时相点(P<0.01),而抑制组虽然也显著高于组内其它时相点(P<0.05),但却显著性低于同时相点对照组的表达水平(P
To investigate the effects of mechanical factors on matrix metalloproteinase9(MMP-9) expressions in rat bone marrow-derived
mesenchymal stem cells(MSCs) and possible mechanism signal.Rat bone marrow MSCs were isolated and cultured,then,exposed to laminar shear stress at
目的:研究p38蛋白激酶(p38MAPK)信号转导通路抑制剂SB202190对体外培养的K562/多柔比星(Dox)耐药细胞表达P-糖蛋白(PGP)的影响。方法:建立PGP高表达的K562/Dox耐药细胞株为对照组。在K562/Dox细胞中加入SB202190为实验组。采用免疫组化学、Western blot和RT-PCR技术检测两组细胞PGP的表达情况;采用四甲基偶氮唑盐法比较两组对苯妥英纳的耐药性。结果:相对于K562/Dox细胞组,给予SB202190后K562/Dox细胞表达PGP水平降低(P
AIM:To
investigate the molecular mechanism and functional consequences of heme oxygenase-1(HO-1) activation by lansoprazole in endothelial cells and macrophages. METHODS:Expression of HO-1 mRNA was analyzed by Northern blotting.Western blotting was used to determine the HO-1 and ferritin protein levels. NADPH-dependent reactive oxygen species(ROS) formation was measured with lucigenin-enhanced chemiluminescence.HO-1 promoter activity in mouse fibroblasts,stably transfected with a 15-kb HO-1 gene that drives expression of the reporter gene luciferase, was assessed 还有 using in vivo bioluminescence imaging. RESULTS:Lansoprazole 许多 increased HO-1 mRNA levels in endothelial cells and HO-1 protein levelsin macrophages.In addition,lansoprazole-induced ferritin protein levels in both cell
systems.Moreover, induction of the antioxidant proteins HO-1 and ferritin by lansoprazole was followed by a decrease in NADPH- mediated ROS formation.The radical scavenging properties of lansoprazole were diminished in the presence of the HO inhibitor,chromium mesoporphyrin IX.Induction of HO-1 gene expression by lansoprazole was not related to oxidative stress or to the activation of the mitogen-activated protein kinase pathway. However,the phosphatidylinositol 3-kinase inhibitor LY294002 showed a concentration-dependent inhibition of HO-1 mRNA and promoter activity. CONCLUSION:Activation of HO-1 and ferritin may account for the gastric protection of lansoprazole and is dependent on a pathway blocked by LY294002.
目的探讨补阳还五汤对脑缺血再灌注损伤的治疗作用及机制。方法88只雄性蒙古沙鼠随机分成对照组、模型组、补阳还五汤高、低剂量组。据Kirino法制作沙鼠前脑缺血模型。术后1、6h,1、3、7d尼氏染色观察海马区神经细胞组织形态变化,Western印迹法检测海马区磷酸化p38MAPK的表达,TUNEL法检测凋亡细胞,术后7～13d八臂迷宫法测试动物学习记忆功能。结果与对照组比较,脑缺血后海马区神经元结构损伤明显、磷酸化p38MAPK表达水平、凋亡神经细胞数量增加(P<0.05);大鼠的学习记忆功能下降;与模型组比较,补阳还五汤组大鼠的学习记忆功能得到改善、神经元形态结构损伤减轻、磷酸化p38MAPK蛋白以及神经细胞凋亡数量回降,上述变化在高剂量补阳还五汤组更为明显(P<0.