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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 reveal the protective mechanism of Naomaitong in the treatment of senile cerebral ischemia-reperfusion injury by the changes of nuclear factor-κB (NF-κB), heat shock protein (HSP70) and nitric oxide synthase (eNOS, iNOS, nNOS) expression. Methods MCAO was used to replicate animal models of cerebral ischemia. Neurological symptom scores, brain tissue water content, pathological changes, and NF-reactivity in rats with cerebral ischemia (I) 3h and reperfusion (I/R) 1, 3, 6 and 12 days were observed. Changes in expression of kappa B, HSP70, and NOS. Results Brain water content in model group (I/R1, 3, 6d), neurotic symptom scores (at each time point), NF-κB (I3h and I/R1, 3d), HSP70 (I/R1, 3, 6, 12d) The expression of eNOS (I/R1, 3, 6d), nNOS (each time point) and iNOS (I/R1, 3, 6d) was higher than that of sham operation group; Water (I/R3, 6, 12d), NF-κB (I/R1, 3, 6, 12d), nNOS (I3h and I/R1, 3d), iNOS (I/R1, 3d) were lower than the model The expression of HSP70 (I/R1, 3, 6, 12d) and eNOS (I/R1, 3, 6d) was higher than that of the model group; neurological symptom scores (I/R6, 12d) and nNOS (INOS) of the Naomai Tongmai group. The expression of /R1d) and iNOS (I/R1d) was lower than that of nimodipine, and eNOS (I/R1d) was higher than that of nimodipine. Conclusion The mechanism of Naomaitong against cerebral ischemia-reperfusion injury is related to inhibiting the expression of NF-κB, nNOS, iNOS and up-regulating the expression of HSP70 and eNOS.