血管性痴呆大鼠的炎症损伤机制及罗格列酮的保护作用

Inflammatory damage mechanism of vascular dementia rats and the protection of rosiglitazone

目的探讨血管性痴呆大鼠炎症损伤机制及罗格列酮对血管性痴呆大鼠炎性细胞因子TNF-α、IL-1β、IL-8表达的影响。方法采用2-血管阻断方法制作血管性痴呆模型。随机分为正常组、假手术组、模型组、罗格列酮治疗组。Morris水迷宫实验检测大鼠的空间学习以及记忆能力;ELISA法检测大鼠海马区TNF-α、IL-1β、IL-8表达。结果 (1)与正常组相比,模型组、治疗组海马区TNF-α、IL-1β、IL-8表达明显升高(P<0.05)。(2)与模型组相比,治疗组的行为学症状较模型组明显改善,治疗组海马区TNF-α、IL-1β、IL-8表达明显下降(P<0.05)。结论炎症反应在血管性痴呆的发生中起到重要的作用。罗格列酮能改善血管性痴呆大鼠的行为学症状,罗格列酮可能是通过降低炎性因子(如TNF-α、IL-1β、IL-8等)抑制炎症反应的途径发挥脑保护作用,使血管性痴呆症状得到改善。

Objective To observe the influence of rosiglltazone on the expressions of TNF-α, IL-1β, IL-8 in rats with vas- cular dementia, so as to study the inflammation damage mechanism of vascular dementia and the neuroprotectlve mechanism of rosiglitazone for vascular dementia. Methods An animal model of vascular dementia was established by two-vessel occlusion. Animals were randomly divided into normal group, sham operation group, model group, rosiglitazone group, The behaviors of animals were tested with Morris water maze. Enzyme linked immunosorbent assay （ELISA） was used to observe the expression of TNF-α, IL-1β, IL-8 in hippocampus. Results Compared to normal group, the learning and memory of model group, rosiglitazone group were lower compared with normal group（P〈0.01）, there was no difference between sham operation group and normal group（P〉0.05）. The expressions of TNF-α, IL-1β, IL-8 in model group, rosiglitazone group were higher（P〈0.01）. Compared to model group, the learning and memory of rosiglitazone group were improved. The expressions of TNF-α, IL-1β, IL-8 in rosiglitazone group were lower （P〈0.05）. Conclusion Inflammatory reaction plays an important role in the develop- ment of vascular dementia. Rosiglitazone can improve the learning and memory in VD rats, its effects may be correlated with the decrease in hippocampal inflammatory mediator （TNF-α, IL-1β, IL-8）.