Hydrogen Sulfide Reduces Cognitive Impairment in Rats After Subarachnoid Hemorrhage by Ameliorating Neuroinflammation Mediated by the TLR4/NF-κB Pathway in Microglia
Hydrogen Sulfide Reduces Cognitive Impairment in Rats After Subarachnoid Hemorrhage by Ameliorating Neuroinflammation Mediated by the TLR4/NF-κB Pathway in Microglia
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DOI：
10.3389/fncel.2020.00210
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发表时间：
2020-07-09
影响因子：
5.3
通讯作者：
Zhang, Jiayong
中科院分区：
文献类型：
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作者：
Duan, Hongzhou;Li, Liang;Zhang, Jiayong
背景与目的：认知障碍是蛛网膜下腔出血（SAH）的主要并发症之一，与神经炎症密切相关。硫化氢（H2S）已被证明具有抗炎作用并减少神经退行性疾病的认知障碍，但其在SAH中的作用研究甚少。本研究旨在探讨H2S对SAH后认知功能障碍的影响及其可能的机制。方法：雄性SD大鼠48只，随机分为假手术组、SAH组、SAH + NaHS （H2S供体）组。采用血管内穿孔技术建立实验性SAH模型。NaHS腹腔注射。采用主动回避测试（AAT）考察认知功能。Western blot和免疫组织化学检测海马组织中tnf - α、toll样受体4 （TLR4）和nf - κ B p65的表达。双免疫荧光染色检测表达tnf - α的细胞类型。结果：与假手术组比较，SAH组大鼠学习记忆能力受损。此外，SAH组海马中tnf - α、TLR4和NF-kappa B p65的表达升高(p
Background and Aims: Cognitive impairment is one of the major complications of subarachnoid hemorrhage (SAH) and is closely associated with neuroinflammation. Hydrogen sulfide (H2S) has been shown to have an anti-inflammatory effect and reduce cognitive impairment in neurodegenerative diseases, but its effects in SAH have been little studied. This study aimed to investigate the effects of H2S on cognitive impairment after SAH and the possible underlying mechanisms.Methods: Forty-eight male Sprague-Dawley (SD) rats were randomly divided into three groups: a sham group, a SAH group, and a SAH + NaHS (an H2S donor) group. The endovascular perforation technique was used to establish the experimental SAH model. NaHS was administered intraperitoneally. An active avoidance test (AAT) was performed to investigate cognitive function. The expression of TNF-alpha, toll-like receptor 4 (TLR4), and NF-kappa B p65 in the hippocampus was measured by Western blot and immunohistochemistry. The types of cells expressing TNF-alpha were detected by double immunofluorescence staining.Results: Compared to that in the sham group, the learning and memory ability of rats in the SAH group was damaged. Furthermore, the expression of TNF-alpha, TLR4, and NF-kappa B p65 in the hippocampus was elevated in the SAH group (p