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目的从肿瘤坏死因子-α(TNF-α)、粘附分子(ICAM-1、VCAM-1)表达变化揭示补阳还五汤抗老年脑缺血再灌注损伤的机制。方法采用大脑中动脉栓塞(MCAO)方法复制脑缺血动物模型,观察缺血(I)3h和缺血再灌注(I/R)1,3,6,12d神经症状积分、脑组织含水量、病理变化、TNF-α、VCAM-1、ICAM-1和ICAM-1mRNA表达变化。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)和TNF-α、VCAM-1(I3h、I/R1,3,6d)、ICAM-1(I3h、I/R1,3,6d)及其mRNA(各时间点)均高于假手术组;补阳还五汤组神经症状积分、脑组织含水量(I/R3,6,12d)、TNF-α、VCAM-1和ICAM-1及其mRNA(I3h、I/R1,3d)表达均低于模型组;补阳还五汤组神经症状积分(I/R6,12d)、TNF-α与ICAM-1(I/R1d)及其mRNA(I/R1,3d)表达低于尼莫地平组。结论补阳还五汤抗老年脑缺血再灌注损伤的机制与其抑制TNF-α、VCAM-1、ICAM-1等表达有关。
Objective To investigate the mechanism of Buyang Huanwu Decoction in treating senile cerebral ischemia-reperfusion injury from the changes of tumor necrosis factor-α (TNF-α) and adhesion molecules (ICAM-1, VCAM-1). Methods Cerebral ischemia model was established by MCAO. The neurological scores, brain water content, ischemia, reperfusion (I/R) 1, 3, 6 and 12 days were observed. Pathological changes, TNF-α, VCAM-1, ICAM-1 and ICAM-1 mRNA expression changes. Results Brain tissue water content (I/R1, 3, 6d), neurotic symptom scores (each time point) and TNF-α, VCAM-1 (I3h, I/R1, 3, 6d), ICAM-1 (I3h) in the model group , I/R1, 3, 6d) and their mRNA (at each time point) were higher than those in the sham operation group; neurological symptom scores, brain tissue water content (I/R3, 6, 12d), and TNF- of Buyang Huanwu Decoction group. The expression of α, VCAM-1 and ICAM-1 and their mRNA (I3h, I/R1, 3d) were lower than those in the model group; neurological symptom scores (I/R6, 12d), TNF-α and ICAM in Buyang Huanwu Decoction group. The expression of -1 (I/R1d) and its mRNA (I/R1, 3d) was lower than that of the nimodipine group. Conclusion The mechanism of Buyang Huanwu decoction against cerebral ischemia reperfusion injury is related to the inhibition of TNF-α, VCAM-1, ICAM-1 expression.