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人类患者单次和长时间发作后脑脊液中白细胞介素-1β和白细胞介素-1受体拮抗剂的水平。

Levels of IL-1beta and IL-1ra in cerebrospinal fluid of human patients after single and prolonged seizures.

机构信息

Department of Neurosurgery, Tampere University Hospital, FI-33521 Tampere, Finland.

出版信息

Neuroimmunomodulation. 2010;17(1):19-22. doi: 10.1159/000243081. Epub 2009 Oct 5.

Abstract

BACKGROUND

Experimentally induced seizures are associated with increased production of inflammatory cytokines in the nervous system. Elevated cerebrospinal fluid levels of cytokine interleukin-6 (IL-6) have been found after a single generalized seizure in human patients. After prolonged seizures, levels of IL-6 have been shown to be even higher compared with single seizures. In the present study, we determined the levels of proconvulsive IL-1beta and anticonvulsive IL-1ra in cerebrospinal fluid after single tonic-clonic seizures as well as after prolonged seizures.

METHODS

The levels of cytokines were measured using enzyme-linked immunosorbent assay.

RESULTS

We found that after single seizures, a slight increase in anticonvulsive IL-1ra levels was found; however, after prolonged partial or recurrent tonic-clonic seizures, the levels of IL-1ra were significantly elevated, together with decreased IL-1beta levels.

CONCLUSION

Our results indicate that after severe seizures, the balance between IL-1-type cytokines is changed towards a neuroprotective and anticonvulsive direction with an overproduction of IL-1ra with respect to potentially neurotoxic IL-1beta. This reaction may serve as a defense mechanism of the nervous system against excitotoxic neuronal damage.

摘要

背景

实验性诱导的癫痫发作与神经系统中炎症细胞因子的产生增加有关。在人类患者单次全身性癫痫发作后,已发现脑脊液中细胞因子白细胞介素-6(IL-6)水平升高。在长时间的癫痫发作后,IL-6 的水平与单次癫痫发作相比甚至更高。在本研究中,我们确定了单次强直阵挛性癫痫发作后以及长时间癫痫发作后脑脊液中促惊厥性白细胞介素-1β(IL-1β)和抗惊厥性白细胞介素-1受体拮抗剂(IL-1ra)的水平。

方法

使用酶联免疫吸附测定法测量细胞因子的水平。

结果

我们发现,单次癫痫发作后,抗惊厥性 IL-1ra 水平略有升高;然而,在长时间的部分或复发性强直阵挛性癫痫发作后,IL-1ra 水平显著升高,同时 IL-1β水平降低。

结论

我们的结果表明,在严重癫痫发作后,IL-1 型细胞因子之间的平衡向神经保护性和抗惊厥性方向转变,IL-1ra 的过度产生相对于潜在的神经毒性 IL-1β。这种反应可能是神经系统对抗兴奋毒性神经元损伤的防御机制。

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