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尼莫地平可改善血管性痴呆大鼠海马区的局部脑血流并抑制炎症因子。

Nimodipine improves regional cerebral blood flow and suppresses inflammatory factors in the hippocampus of rats with vascular dementia.

作者信息

Zhang X-L, Zheng S-L, Dong F-R, Wang Z-M

机构信息

Department of Radiology, First Affiliated Hospital of Liaoning Medical College, Jinzhou, Liaoning Province, China.

出版信息

J Int Med Res. 2012;40(3):1036-45. doi: 10.1177/147323001204000322.

DOI:10.1177/147323001204000322
PMID:22906276
Abstract

OBJECTIVE

To study the effect of nimodipine on hippocampal regional cerebral blood flow (rCBF) and proinflammatory cytokines in rats with experimental vascular dementia.

METHODS

Male Sprague Dawley rats were randomly divided into four groups (n = 15/group): sham operated controls (group A); focal cerebral ischaemia (group B); vascular dementia (group C); and vascular dementia treated with 20 mg/kg nimodipine daily (group D). The Morris water maze test evaluated learning and memory, and magnetic resonance perfusion-weighted imaging was used to measure rCBF. Hippocampal levels of nuclear factor-κB (NF-κB), tumour necrosis factor-α (TNF-α) and interleukin 1β (IL-1β) were measured.

RESULTS

Compared with group C, rats in group D demonstrated significantly improved learning ability and significantly increased hippocampal rCBF. The levels of NF-κB, TNF-α and IL-1β were significantly lower in group D than in group C. Hippocampal nerve cell morphology was abnormal in group C but near normal in group D.

CONCLUSIONS

Nimodipine improved the symptoms of cognitive impairment, increased rCBF, reduced hippocampal cytokine levels and alleviated neuronal injury in the hippocampus of rats with experimental vascular dementia.

摘要

目的

研究尼莫地平对实验性血管性痴呆大鼠海马区局部脑血流量(rCBF)及促炎细胞因子的影响。

方法

雄性Sprague Dawley大鼠随机分为四组(每组n = 15):假手术对照组(A组);局灶性脑缺血组(B组);血管性痴呆组(C组);每日给予20 mg/kg尼莫地平治疗的血管性痴呆组(D组)。采用Morris水迷宫试验评估学习和记忆能力,磁共振灌注加权成像测量rCBF。检测海马区核因子-κB(NF-κB)、肿瘤坏死因子-α(TNF-α)和白细胞介素1β(IL-1β)水平。

结果

与C组相比,D组大鼠学习能力显著改善,海马rCBF显著增加。D组NF-κB、TNF-α和IL-1β水平显著低于C组。C组海马神经细胞形态异常,而D组接近正常。

结论

尼莫地平改善了实验性血管性痴呆大鼠的认知障碍症状,增加了rCBF,降低了海马细胞因子水平,减轻了海马神经元损伤。

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