NF-κB和HSP70在失血性休克肝枯否细胞中的活性变化研究

Activation changes of NF-κB and HSP70 in liver kupffer cells by hemorrhagic shock

目的探讨NF-κB和HSP70在失血性休克诱发肝脏损伤中的活性变化和相互影响机制。方法采用原位杂交(ISH)、凝胶电泳迁移率改变分析(EMSA)方法检测失血性休克家兔模型动物休克后不同时间点(2、6、12、24h)肝脏枯否细胞(KC)中HSP70 mRNA表达和NF-κB活性变化。结果休克动物NF-κB活性于2h已升高(0.722±0.115)、6h升高最明显(1.163±0.229)、12h开始下降(0.732±0.229)、24h下降到最低点(0.512±0.102);而HSP70 mRNA表达2h(0.088±0.013)开始升高、6h(0.125±0.019)逐渐升高、12h(0.161±0.011)至24h(0.185±0.039)增高最为显著。结论失血性休克肝脏炎症损伤过程中NF-κB活化可能受到体内HSP70活性变化的抑制调控。

Objective To explore the level of NF - KB and HSP70 in the liver damage induced by hemorrhagic shock and the mechanism of their mutual regulation. Methods In - situ hybridization （ISH） was used to detect HSP70 mRNA expression and electrophoretic mobility shift assay （EMSA） was used to detect activities of NF - kB in liver kupffer cells （ KCs ） of rabbit model of hemorrhagic shock at 2, 6, 12, 24 h respectively. Results NF- kB activity was elevated at 2 h （0. 722 ± 0.115） , with the highest level at 6 h （ 1. 163 ± 0. 229 ）. It decreased at 12 h （ 0. 732 ± 0. 229 ） , with the lowest level at 24 h （0.512 ± 0. 102 ）. Meanwhile, HSP70 mRNA expression was first increased at 2 h （ 0. 088 ± 0. 013 ） , and was gradually increased with the 6 h level （0. 125 ±0. 019 ） , 12 h level （ 0. 161 ± 0.011 ） , and with the highest level at 24 h （ 0. 185 ±0. 039 ） . Conclusion NF - kB activation might be negatively regulated by HSP70 in the liver damage induced by hemorrhagic shock.