The pathway for p38 MAP kinase phosphorylationis different from that of p44/42 MAP kinase,suggestingthat it piays a different role in the cellular response to IL-1β.
目的 :探讨p38MAPK在介导TNF α所致大鼠胶质瘤细胞C6凋亡中的作用。方法 :应用MTT法检测TNF α处理的C6细胞的增殖活性 ,采用透射电镜和流式细胞仪观察凋亡的发生 ,应用SABC法和Westernblot检测p38MAPK的表达 ,应用流式细胞仪及SABC法观察 p38MAPK特异性抑制剂SB2 0 2 1 90对TNF α诱导C6细胞凋亡的影响。结果 :TNF α(2× 1 0 5U/L)对C6细胞增殖的抑制率为 43 .75 % ,透射电镜下可见典型的凋亡细胞 ,流式细胞仪检测凋亡率为 37.5 % ,SABC法和Westernblot显示P38MAPK表达阳性 ;加入SB2 0 2 1 90后 ,其凋亡率为 7.0 % ,未见P38MAPK表达。结论 :TNF α能诱导C6细胞凋亡和 Compound C p38MAPK表达 ,p38MAPK的活化促进了C6细胞凋亡的发生
目的 研究离体肝脏缺血再灌注期间p38信号转导途径的激活对其损伤程度的影响。 方法 通过自行建立的兔离体肝脏缺血再灌注模型,将一定剂量的特异性p38丝裂原激活蛋白激酶(MAPK)抑制剂SB202190加入到保存液中,根据原位灌注液及保存液中加入SB202190的剂量再将离体肝分为A、B、C、D4组。分别于冷保存前、冷保存末及再灌注5、10、15、30、60、120
min获取离体肝组织及受体兔静脉血液标本。分别应用免疫印迹杂交和免疫沉淀法测定离体肝组织磷酸化p38M A P K的活性。用全自动生化分析仪测定离体兔肝功酶学含量;并测定再灌注120 min内的胆汁分泌总量。 结果 在正常肝组织中p38 MAPK即有一定的基础活性;经冷保存后有一定的升高,再灌注10 min时达到峰值,然后逐渐下降,至再灌注120 min时降低至正常水平,而在冷保存液中加入SB202190后,再灌注期间p38 MAPK的活性受到显著性抑制,其中B、C、D组p38 MAPK活性峰值仅分别为A组的53.9％,12.8％,9.6％;再灌注期间各组受体肝酶学水平均表现为A>B>C>D,而胆汁分泌量表现为A
To study the role of p38MAPK in mediating TNF-α-induced apoptosis of rat glioma cell line C6. Methods: Effect of TNF-α on the proliferation of C6 cells was determined by MTT assay. The TNF-α induced apoptosis was detected by transmission electron microscopy and flow cytometry. The expression of p38MAPK was detected by SABC method and Western-blot. The effect of SB202190,
a specific inhibitor 时间 of p38MAPK, on TNF-α-induced apoptosis was observed by flow cytometry and SABC method. Results: Inhibitory rate of TNF-α(2×105 U/L) on C6 cells was 43. 75% . In the TNF-α treated group, apoptotic cells were observed by transmission electron microscopy and the apoptotic rate was 37. 5% by flow cytometry. p38MAPK positive signals were detected by SABC method and Western-blot. In the SB202190 treated group, the apoptotic rate was 7. 0% and no p38MAPK signals were found. Conclusion: Apoptosis of C6 cells and expression of p38MAPK can be induced by TNF-α. The activation of p38MAPK promotes the apoptosi
AIM:Activated pancreatic stellate cells(PSCs)have beenimplicated 可能 in the pathogenesis of pancreatic fibrosis andinflammation.Primary PSCs can be subcultured only severaltimes because of their limited growth potential.A continuouscell line may therefore be valuable in studying molecularmechanisms of these pancreatic disorders.The aim of thisstudy was to establish a cell line of rat PSCs by spontaneousimmortalization.METHODS:PSCs were isolated from the pancreas of maleWistar rats,and conventional subcultivation was performedrepeatedly.Telomerase activity was measured using thetelomere repeat amplification protocol.Activation of transcriptionfactors was assessed by electrophoretic mobility shift assay.