脓毒症大鼠海马白细胞介素-1β转化酶的表达及其意义

The expression and role of interleutin-1β converting enzyme （ICE） on neuron injury following sepsis in rat hippocampus

目的探讨白细胞介素-1β转化酶在腹腔感染脓毒症致神经元损伤中的机制。方法建立Wistar大鼠腹腔感染脓毒症模型，研究脓毒症后不同时间内海马组织ICE的活性，IL-1β含量变化及海马CA1区神经元计数的变化，同时观察用Ac-YVAD-FMK治疗后对上述指标的影响。结果随着发生脓毒症时间的延长，脑海马组织中ICE活性和IL-1β含量显著升高（P〈0．05和P〈0．01），海马CA1区神经元计数显著降低（P〈0．05和P〈0．01）。使用Ac-YVAD-FMK治疗后上述各指标的异常变化明显减轻，与模型组比差异具有统计学意义（P〈0．05和P〈0．01）。结论脓毒症后ICE主要通过炎症机制介导神经元的损伤，Ac-YVAD-FMK对脓毒症后神经元的损伤具有保护作用。

Objective To investigate the mechanism of ICE inducing neurom injury following sepsis. Method Cecal ligation and puncture （CLP） was used to make a model of abdominal infection in rats for in this study. Sixty-six Male wistar rats were divided randomly into three groups： sham-operated control group （ Ⅰ ）, CLP group（Ⅱ）, and CLP group treated with AC-YVAD-FMK （Ⅲ）. The dynamic changes of ICE （caspase-1） activity and IL-1β content at several phasic points following CLP were observed. The effects of Ac-YVAD FMK （Ⅲ） on above biomarkers were also observed. Results The ICE activity and IL-1β content in hippocampus significantly increased as sepsis persiste, and neruon density in CA1 of hippocampus significantly decreased. In Ac-YVAD-FMK-treated group, the changes of above biomarkers were ameliorated markedly, and there was significant difference between CLP group and Ac-YVAD-FMK group （ P 〈0.05 and P 〈0.01）. Conclusion ICE may get involved in neuron injury after sepsis through inflammation, and Ac-YVAD-FMK could protect the damage to neurons in septic rats.