摘要
目的 观察Ca2+ /钙调蛋白依赖性激酶Ⅱ(Ca2+ /CaMPKⅡ)竞争性抑制剂KN- 93对缺血再灌注损伤后大鼠肾上腺嗜铬细胞瘤细胞(PC12)核因子κB(NF- κB)的表达及细胞活性的影响情况。方法 将传代培养的PC12细胞在特制的装置中进行缺血再灌注处理,建立研究所需要的细胞模型并施以KN- 93进行干预,运用免疫细胞化学和流式细胞仪技术检测不同处理条件下NF- κB的表达情况,并应用甲基噻唑蓝(MMT)比色法对细胞的损伤程度进行检测。结果 经过KN 93预处理的试验组相对于单纯缺血再灌注处理对照组,NF- κB的表达和细胞损伤程度均明显降低(P<0. 01 )。结论 KN 93能够减少缺血再灌注引起的胞浆PC12细胞NF -κB的上调,并能减轻细胞的损伤程度;缺血再灌注损伤中NF κB的激活可能存在着Ca2+ /CaMPKⅡ调控通路。
Objective To observe the effects of KN-93 on nuclear factor κB (NF-κB) expression and cell activity in PC12 cells following ischemia-reperfusion injury.Methods The subculturing PC12 cells encountered ischemia-reperfusion injury with the pretreatment of KN-93 in the special device. The expressions of NF-κB were measured by immunocytochemical method and flow cytometer, and the extent of cells injury was analyzed with methyl thiazolyl tetrazolium (MTT) reduction assay.Results The expression of NF-κB in the KN-93-treated groups was lower than that in the control groups (P<0.01). The value of injured cells in the KN-93-treated groups was significantly higher than that in the control groups (P<0.01).Conclusion It is probable that KN-93 can protect PC12 cells from ischemia-reperfusion injury by down-regulating intracellular NF-κB induced by ischemia-reperfusion, and Ca 2+/calmodulin-dependent protein kinase II (Ca 2+/CaM PKⅡ)may modulate the activation of NF-κB induced by ischemia-reperfusion injury in PC12.
出处
《中华神经外科疾病研究杂志》
CAS
2005年第2期114-117,共4页
Chinese Journal of Neurosurgical Disease Research
基金
杨森科学研究基金资助项目
