Ning Bo, Li Zhen, Ning Lei, Wu Jun, Chen Xin, Jiang Pengjun, Lin Fuxin, Zhao Bing
Department of Neurosurgery, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250021, P.R. China.
Department of Neurosurgery, Guangzhou Red Cross Hospital, Jinan University, Guangzhou, Guangdong 510220, P.R. China.
Exp Ther Med. 2021 Apr;21(4):364. doi: 10.3892/etm.2021.9795. Epub 2021 Feb 18.
Subarachnoid hemorrhage (SAH) is a life-threatening neurological disease. Recently, inflammatory factors have been confirmed to be responsible for the brain damage associated with SAH. Therefore, studying the post-SAH inflammatory reaction may clarify the mechanism of SAH. Mitogen and stress-activated protein kinase 1 (MSK1) causes the phosphorylation of NF-κB and regulates the activity of pro-inflammatory transcription factors. The present study aimed to identify the potential role of MSK1 in inflammation and brain damage development following SAH. A cisterna magna blood injection model was established in Sprague-Dawley rats. Hematoxylin and eosin staining, reverse transcription-quantitative polymerase chain reaction assays and double immunofluorescence staining were used to analyze the role of MSK1, IL-1β and TNF-α in the inflammatory process after SAH. In a model of lipopolysaccharide-induced astrocyte inflammation, the effect of overexpressing MSK1 overexpression was analyzed by western blot analysis. The results demonstrated that MSK1 expression were negatively correlated with TNF-α and IL-1β expression levels, and reached peak levels 2 days after TNF-α and IL-1β. The double immunofluorescence staining results showed that the expression of MSK1 was in the same plane of view as TNF-α and IL-1β in the brain cortex. Furthermore, the studies indicated that the overexpression of MSK1 inhibited the expression of TNF-α and IL-1β following LPS challenge. These results imply that MSK1 may be involved in the inflammatory reaction following SAH, and may potentially serve as a negative regulator of inflammation.
蛛网膜下腔出血（SAH）是一种危及生命的神经系统疾病。最近，炎症因子已被证实与SAH相关的脑损伤有关。因此，研究SAH后的炎症反应可能会阐明SAH的发病机制。丝裂原和应激激活蛋白激酶1（MSK1）可导致NF-κB磷酸化并调节促炎转录因子的活性。本研究旨在确定MSK1在SAH后炎症和脑损伤发展中的潜在作用。在Sprague-Dawley大鼠中建立了枕大池注血模型。采用苏木精-伊红染色、逆转录-定量聚合酶链反应分析和双重免疫荧光染色来分析MSK1、IL-1β和TNF-α在SAH后炎症过程中的作用。在脂多糖诱导的星形胶质细胞炎症模型中，通过蛋白质免疫印迹分析来分析过表达MSK1的作用。结果表明，MSK1的表达与TNF-α和IL-1β的表达水平呈负相关，且在TNF-α和IL-1β之后2天达到峰值水平。双重免疫荧光染色结果显示，在大脑皮层中，MSK1的表达与TNF-α和IL-1β处于同一视野平面。此外，研究表明，MSK1的过表达在脂多糖刺激后抑制了TNF-α和IL-1β的表达。这些结果表明，MSK1可能参与SAH后的炎症反应，并可能作为炎症的负调节因子。
