脑脉通对老龄大鼠脑缺血再灌注核转录因子NF-κB和一氧化氮合酶的影响

Influence of Naomaitong Granules on NF-κB and NOS in aged rats with cerebral ischemia reperfusion injury

目的从核转录因子κB(NF-κB)、热休克蛋白(HSP70)和一氧化氮合酶(eNOS、iNOS、nNOS)表达的变化揭示脑脉通抗老年脑缺血再灌注损伤的保护机制。方法采用MCAO方法复制脑缺血动物模型,观察脑缺血(I)3h和再灌注(I/R)1、3、6、12d大鼠神经症状积分、脑组织含水量、病理变化、NF-κB、HSP70和NOS表达的变化。结果模型组脑组织含水量(I/R1、3、6d),神经症状积分(各时间点),NF-κB(I3h和I/R1、3d),HSP70(I/R1、3、6、12d),eNOS(I/R1、3、6d)、nNOS(各时间点)和iNOS(I/R1、3、6d)的表达均高于假手术组;脑脉通组神经症状积分,脑组织含水量(I/R3、6、12d),NF-κB(I/R1、3、6、12d),nNOS(I3h和I/R1、3d)、iNOS(I/R1、3d)的表达低于模型组,HSP70(I/R1、3、6、12d)和eNOS(I/R1、3、6d)的表达高于模型组;脑脉通组神经症状积分(I/R6、12d)和nNOS(I/R1d)、iNOS(I/R1d)的表达低于尼莫地平组,eNOS(I/R1d)高于尼莫地平组。结论脑脉通抗脑缺血再灌注损伤的机制与抑制NF-κB、nNOS、iNOS表达和上调HSP70、eNOS表达有关。

Objective To explore the mechanism of antagonizing senile cerebral ischemia reperfusion injury of Naomaitong Granules by observing the expression changes of nucleotranscript factor-kB （NF- kB） , heat shock protein 70 （HSP70） , and nitric oxide synthases （ eNOS, iNOS and nNOS） in aged rats with cerebral ischemia reperfusion injury. Methods The animal model of cerebral ischemia was copied by middle cerebral artery occlusion （MCAO） method. The nerve dysfunction score, water content of brain, pathological changes, expressions of NF-kB, HSP70 and NOS were observed respectively 3 hours after cerebral ischemia and on thel st, 3rd, 6th and 12th day after the I/Rmodel establishment. Results In the model group water content of brain （ I/R 1, 3 and 6d）, nerve dysfunction score （different time points）, the expressions of NF-KB （I 3 h, I/R 1 and 3 d） , HSP70 （I/R 1,3, 6 and 12 d） , eNOS （If R 1, 3 and 6 d）, nNOS （different time points）, iNOS （I/R 1,3 and 6 d） were all higher than those in the sham-operation group. In the Naomaitong Granules group the nerve dysfunction score, water content of brain （I/R 3, 6 and 12 d） , expressions of NF-KB （I/R 1,3, 6 and 12 d）, nNOS （I 3h, I/R 1 and 3 d） and iNOS （I/R 1 and 3 d） were all lower than those in the model group, while the expressions of HSP70 （I/R 1,3, 6 and 12 d） and eNOS （I/R 1,3 and 6 d） were higher. In the Naomaitong Granules group the nerve dysfunction score （I/R 6 and 12 d）, the expressions of nNOS （I/R 1 d） and iNOS （I/ R 1 d） were lower than those in the nimodipine group, while the expression of eNOS （I/R 1 d） was higher. Conclusion The mechanism of Naomaitong Granules for antagonizing cerebral isehemia reperfusion injury is related to that it can inhibit the expressions of NF-kB, nNOS and iNOS, and upregulate the expressions of HSP70 and eNOS.