摘要
目的探讨核转录因子-kB(NF-kB)在缺血致神经元损伤中的作用。方法建立 Wistar 大鼠全脑缺血/再灌注模型。研究脑缺血10 min 后不同再灌注时间内海马组织 NF-kB 的活性,TNF-α含量变化,脑组织含水量的变化,同时观察用 PDTC 治疗后对上述指标的影响。结果随再灌注时间的延长,脑海马组织中 NF-kB 活性、TNF-α含量,脑组织水含量显著升高(P<0.05和 P<0.01)。使用 NF-kB 特异性抑制剂 PDTC 治疗后,上述各指标的异常变化明显减轻,与损伤组比有显著性差异(P<0.05和 P<0.01)。结论全脑缺血/再灌注后,海马出现 NF-kB 的表达且活性增高,同时伴有炎性细胞因子 TNF-α含量增加,脑水含量增加,提示 NF-kB 的活化参与了脑缺血神经元的损伤,应用 NF-kB 特异性抑制剂能减轻脑缺血神经元的损伤。
Objective To investigate whether NF-κB may be involve in neuron injury and what is the mechanism it may play after complete cerebral ischemia/reperfusio. Methods A model of rats with four vessels occluded which induced global ischemia was used in this study. Male wister rats were divided randomly into three group. (Ⅰ) Sham-operated control group. ( Ⅱ ) Cerebral ischemia and ( Ⅲ ) cerebral ischemia group treated with PDTC( PDTC group). We observed the changes of NF-κB activity,TNF-α content and brain edema at several phasic points following cerebral ischemia/reperfusion. The treatment of PDTC ( Ⅲ ) on above changes was observed also. Results The NF-κB activity, TNF-α content in hippocampus increased apparently, and the brain edema also increased apparently ( P 〈 0. 05 and P 〈 0. 01 ), in PDTC-treating group, the abnormal change indeses as above were ame-lorated markedly, and there was significant difference between IR group and PDTC group( P 〈0. 05 and P 〈0. 01 ). Conclusion With active TNF-α content increasing, NF-κB activity of hippocampus after ischemia/reperfusion increased, the brain edema increased also, all the changes decreased apparently with treatment of PDTC ,which suggested that NF-κB might get involved in neuron injury after ischemia/reperfusion.
出处
《临床急诊杂志》
CAS
2008年第1期7-9,12,共4页
Journal of Clinical Emergency