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Inflammatory markers in the hippocampus after audiogenic kindling

机译:发起疗作用后海马的炎症标志物

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摘要

Here, we investigated the participation of pro and anti-inflammatory cytokines in the spread of repeated audiogenic seizures from brainstem auditory structures to limbic areas, including the hippocampus. We used Wistar Audiogenic Rats (WARS) and Wistars submitted to the audiogenic kindling protocol with a loud broad-band noise. We measured pro and anti-inflammatory cytokines and nitrate levels in the hippocampus of stimulated animals. Our results show that all WARS developed audiogenic seizures that evolved to limbic seizures whereas seizure-resistant controls did not present any seizures. However, regardless of seizure severity, we did not observe differences in the pro inflammatory cytokines IL-1 beta, IL-6, TNF-alpha and IFN-alpha or in the anti-inflammatory IL-10 in the hippocampi of audiogenic and resistant animals. We also did not find any differences in nitrate content. Our data indicate that the spread of seizures during the audiogenic kindling is not dependent on hippocampal release of cytokines or oxidative stress, but the severity of brainstem seizures will be higher in animals with higher levels of cytokines and the oxidative stress marker, nitrate.
机译:在这里,我们调查了Pro和抗炎细胞因子在脑干听觉结构到肢体区域的重复发作性癫痫发作中的参与,包括海马。我们使用Wistar Audiogenic大鼠(WARS)和Wistars提交给发声点燃协议,响亮的宽带噪音。我们在刺激动物的海马中测量了Pro和抗炎细胞因子和硝酸盐水平。我们的研究结果表明,所有战争都开发了演变为肢体癫痫发作的发声癫痫发作,而耐癫痫管道未呈现任何癫痫发作。但是,无论癫痫发作严重程度如何,我们都没有观察到促炎症和抗性动物海马的促炎细胞因子IL-1β,IL-6,TNF-α和IFN-α或抗炎IL-10中的差异。我们还没有发现硝酸盐内容的任何差异。我们的数据表明,在发起毒性的癫痫发作期间的癫痫发作不依赖于细胞因子或氧化应激的海马释放,但脑干癫痫发作的严重程度将在具有更高水平的细胞因子和氧化应激标记物,硝酸盐的动物中更高。

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