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大鼠脑缺血栓塞模型中的促炎细胞因子

Proinflammatory cytokines in the embolic model of cerebral ischemia in rat.

作者信息

Jafarinaveh Hamid Reza, Allahtavakoli Mohammad, Rezazadeh Hossein, Kazemi Arababadi Mohammad, Taghavi Mohammad Mohsen, Shamsizadeh Ali, Rahmani Mohammad Reza

机构信息

Department of Anatomy, School of Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.

出版信息

Iran J Allergy Asthma Immunol. 2014 Apr;13(2):125-30.

PMID:24338258
Abstract

Increased levels of proinflammatory cytokines have been recorded after the onset of transient or permanent brain ischemia and are usually associated with exacerbation of ischemic injury. Embolic stroke model is more relevant to the pathophysiological situation in such patients, because the majority of ischemic injuries in humans are induced by old thrombi that originate from the heart and carotid arteries. Therefore, the aim of the present study was to investigate changes of inflammatory cytokines after embolic stroke. Rats were subjected to embolic stroke, induced by a natural old clot which was injected in Middle Cerebral Artery (MCA), or sham stroke, which the same volume of saline was injected into the MCA. At 48 h after stroke induction, the levels of 5 cytokines (IL-1α and β, IL-6, IFN-γ and TNF-α) were determined in 500 µg of total protein using the Bio-Plex Rat Cytokine Array (BioRad), according to the manufacturer's instructions in ischemic and non-ischemic cortices. While stroke animals showed infarctions and neurological deficits, we did not observe any cerebral infarction and neurological deficits in sham-operated animals. The levels of IL-1α (p=0.000) and -β (p =0.004), IL-6 (p =0.008), TNF-α (p =0.000) and IFN-γ (p =0.044) were significantly increased compared to sham treated animals. The findings of the present study suggest that part of ischemic injury in the embolic stroke may be mediated through the increased levels of inflammatory cytokines.

摘要

短暂性或永久性脑缺血发作后,促炎细胞因子水平会升高,且通常与缺血性损伤的加重有关。栓塞性中风模型与这类患者的病理生理情况更为相关,因为人类的大多数缺血性损伤是由源自心脏和颈动脉的陈旧血栓引起的。因此,本研究的目的是调查栓塞性中风后炎症细胞因子的变化。大鼠接受栓塞性中风,通过将天然陈旧血凝块注入大脑中动脉(MCA)诱导而成,或接受假中风,即将相同体积的生理盐水注入MCA。在中风诱导后48小时,根据制造商的说明,使用Bio-Plex大鼠细胞因子阵列(BioRad)在缺血和非缺血皮质的500μg总蛋白中测定5种细胞因子(IL-1α和β、IL-6、IFN-γ和TNF-α)的水平。中风动物出现梗死和神经功能缺损,而假手术动物未观察到任何脑梗死和神经功能缺损。与假处理动物相比,IL-1α(p = 0.000)和-β(p = 实验结果显示,栓塞性中风中部分缺血性损伤可能通过炎症细胞因子水平升高介导。 0.004)、IL-6(p = 0.008)、TNF-α(p = 0.000)和IFN-γ(p = 0.044)的水平显著升高。本研究结果表明,栓塞性中风中部分缺血性损伤可能通过炎症细胞因子水平升高介导。

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