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吲哚美辛可以下调匹罗卡品诱导的癫痫持续状态大鼠海马中炎症介质的水平。

Indomethacin can downregulate the levels of inflammatory mediators in the hippocampus of rats submitted to pilocarpine-induced status epilepticus.

作者信息

Vieira Michele Juliane, Perosa Sandra Regina, Argaãaraz Gustavo Adolfo, Silva José Antônio, Cavalheiro Esper Abrão, Graça Naffah-Mazzacoratti Maria da

机构信息

Departamento de Neurologia/Neurocirurgia, Universidade Federal de São Paulo, São Paulo, SP, Brazil.

Laboratório de Patologia Molecular, Faculdade de Ciências da Saúde, Universidade de Brasília, Brasilia, DF, Brazil.

出版信息

Clinics (Sao Paulo). 2014 Sep;69(9):621-6. doi: 10.6061/clinics/2014(09)08.

DOI:10.6061/clinics/2014(09)08
PMID:25318094
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4192421/
Abstract

OBJECTIVE

Refractory status epilepticus is one of the most life-threatening neurological emergencies and is characterized by high morbidity and mortality. Additionally, the use of anti-inflammatory drugs during this period is very controversial. Thus, this study has been designed to analyze the effect of a low dose of indomethacin (a COX inhibitor) on the expression of inflammatory molecules.

METHOD

The hippocampus of rats submitted to pilocarpine-induced long-lasting status epilepticus was analyzed to determine the expression of inflammatory molecules with RT-PCR and immunohistochemistry.

RESULTS

Compared with controls, reduced levels of the kinin B2 receptors IL1β and TNFα were found in the hippocampus of rats submitted to long-lasting status epilepticus and treated with indomethacin.

CONCLUSIONS

These data show that low doses of indomethacin could be employed to minimize inflammation during long-lasting status epilepticus.

摘要

目的

难治性癫痫持续状态是最危及生命的神经急症之一，具有高发病率和高死亡率的特点。此外，在此期间使用抗炎药物存在很大争议。因此，本研究旨在分析低剂量吲哚美辛（一种环氧化酶抑制剂）对炎症分子表达的影响。

方法

对接受匹鲁卡品诱导的长期癫痫持续状态的大鼠海马进行分析，采用逆转录聚合酶链反应（RT-PCR）和免疫组织化学方法测定炎症分子的表达。

结果

与对照组相比，接受长期癫痫持续状态并接受吲哚美辛治疗的大鼠海马中缓激肽B2受体、白细胞介素1β（IL1β）和肿瘤坏死因子α（TNFα）的水平降低。

结论

这些数据表明，低剂量吲哚美辛可用于在长期癫痫持续状态期间将炎症降至最低。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/2042bf0fdfaa/cln-69-09-621-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/b26de1ac1df1/cln-69-09-621-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/99b17e229466/cln-69-09-621-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/638ffa650ee9/cln-69-09-621-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/b8a4e404db44/cln-69-09-621-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/2042bf0fdfaa/cln-69-09-621-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/b26de1ac1df1/cln-69-09-621-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/99b17e229466/cln-69-09-621-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/638ffa650ee9/cln-69-09-621-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/b8a4e404db44/cln-69-09-621-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/11e9/4192421/2042bf0fdfaa/cln-69-09-621-g005.jpg

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