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锌-α2-糖蛋白过表达抑制戊四氮点燃大鼠的癫痫发作和癫痫相关神经炎症。

Overexpression of zinc-α2-glycoprotein suppressed seizures and seizure-related neuroflammation in pentylenetetrazol-kindled rats.

机构信息

Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, 74 Linjiang Road, Yuzhong District, Chonqing, 400010, China.

Department of Neurosurgery, The University-Town Hospital of Chongqing Medical University, Chongqing, 401331, China.

出版信息

J Neuroinflammation. 2018 Mar 22;15(1):92. doi: 10.1186/s12974-018-1132-6.

DOI:10.1186/s12974-018-1132-6
PMID:29566716
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5863804/
Abstract

BACKGROUND

Zinc-α2-glycoprotein (ZAG) is a 42-kDa protein reported as an anti-inflammatory adipocytokine. Evidences from clinical and experimental studies revealed that brain inflammation plays important roles in epileptogenesis and seizure. Interestingly, closely relationship between ZAG and many important inflammatory mediators has been proven. Our previous study identified ZAG in neurons and found that ZAG is decreased in epilepsy and interacts with TGFβ and ERK. This study aimed to investigate the role of ZAG in seizure and explore its effect on seizure-related neuroinflammation.

METHODS

We overexpressed AZGP1 in the hippocampus of rats via adeno-associated virus vector injection and observed their seizure behavior and EEG after pentylenetetrazol (PTZ) kindling. The level of typical inflammation mediators including TNFα, IL-6, TGFβ, ERK, and ERK phosphorylation were determined.

RESULTS

The overexpression of AZGP1 reduced the seizure severity, prolonged the latency of kindling, and alleviated epileptiform discharges in EEG changes induced by PTZ. Overexpression of AZGP1 also suppressed the expression of TNFα, IL-6, TGFβ, and ERK phosphorylaton in PTZ-kindled rats.

CONCLUSIONS

ZAG may inhibit TGFβ-mediated ERK phosphorylation and inhibit neuroinflammation mediated by TNFα and IL-6, suggesting ZAG may suppress seizure via inhibiting neuroinflammation. ZAG may be a potential and novel therapeutic target for epilepsy.

摘要

背景

锌-α2-糖蛋白（ZAG）是一种 42kDa 的蛋白，被报道为一种抗炎脂肪细胞因子。临床和实验研究的证据表明，脑炎症在癫痫发生和发作中起着重要作用。有趣的是，已经证明 ZAG 与许多重要的炎症介质密切相关。我们之前的研究在神经元中鉴定出了 ZAG，并发现 ZAG 在癫痫中减少，并且与 TGFβ 和 ERK 相互作用。本研究旨在探讨 ZAG 在癫痫发作中的作用，并研究其对与癫痫相关的神经炎症的影响。

方法

我们通过腺相关病毒载体注射在大鼠海马中过表达 AZGP1，并在戊四氮（PTZ）点燃后观察其癫痫发作行为和脑电图。测定了 TNFα、IL-6、TGFβ、ERK 和 ERK 磷酸化等典型炎症介质的水平。

结果

AZGP1 的过表达降低了癫痫发作的严重程度，延长了点燃的潜伏期，并减轻了 PTZ 诱导的脑电图变化中的癫痫样放电。AZGP1 的过表达还抑制了 PTZ 点燃大鼠中 TNFα、IL-6、TGFβ 和 ERK 磷酸化的表达。

结论

ZAG 可能抑制 TGFβ 介导的 ERK 磷酸化，并抑制 TNFα 和 IL-6 介导的神经炎症，提示 ZAG 可能通过抑制神经炎症来抑制癫痫发作。ZAG 可能是一种有潜力的新型癫痫治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/1ed035ff877a/12974_2018_1132_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/565b6a49c5d3/12974_2018_1132_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/5497f84932cc/12974_2018_1132_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/ac40d72c9f13/12974_2018_1132_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/58981406028a/12974_2018_1132_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/1ed035ff877a/12974_2018_1132_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/565b6a49c5d3/12974_2018_1132_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/5497f84932cc/12974_2018_1132_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/ac40d72c9f13/12974_2018_1132_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/58981406028a/12974_2018_1132_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c457/5863804/1ed035ff877a/12974_2018_1132_Fig5_HTML.jpg

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