Intracerebral haemorrhage (ICH) is a lethal cerebrovascular disorder with a high mortality and morbidity. Although it is a major public health problem, there is no effective treatment for ICH. After ICH, the primary and secondary mechanisms are mentioned when discussing brain injury. The transcription factor, nuclear factor-kappa B (NF-kB), is an important regulator of inflammatory responses. The role of platelet factor 4 (PF4) in ICH is unclear. To study the effect of PF4 on inflammatory response of rats in ICH, a rat model of striatum ICH was established by injecting autologous blood from the autogenous femoral artery into the right striatum of rats. Forty-eight hours after ICH, the expression of PF4, NF-kB (P-P65) and inflammatory changes in rats were determined with WB and ELISA. Heme was used to induce PC12 cell damage, simulate

the ICH model in vitro, and detect PF4, P-P65 and striatal inflammatory changes. Short hairpin RNA (shRNA-PF4) was used to knock-down the expression of PF4 in PC12 cells to detect changes in inflammatory factors. The results showed that 48 hours after surgery, the behavioural score of cerebral haemorrhage was the lowest. The expression of PF4 and P-P65 in the striatum of the ICH group was significantly higher compared with the sham surgery group. The expression of interleukin (IL)-6 and IL-1b in the ICH group was also greatly improved. After inhibiting NF-kB expression, PF4 expression was decreased. In short, ICH enhances the expression of PF4, which induces an inflammatory response in rats with cerebral haemorrhage through the NF-kB signalling pathway. Reducing the expression of PF4 can attenuate the inflammatory response.

中文翻译：

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PF4通过NF-kB信号通路诱导脑出血大鼠炎症反应

脑出血（ICH）是一种致命性脑血管疾病，具有很高的死亡率和发病率。尽管ICH是一个重大的公共卫生问题，但目前尚无有效的治疗方法。ICH 之后，在讨论脑损伤时会提到主要和次要机制。转录因子核因子 kappa B (NF-kB) 是炎症反应的重要调节因子。血小板因子 4 (PF4) 在 ICH 中的作用尚不清楚。为研究PF4对脑出血大鼠炎症反应的影响，通过自体股动脉向大鼠右侧纹状体注射自体血，建立纹状体脑出血大鼠模型。ICH后48小时，采用WB和ELISA测定大鼠PF4、NF-kB（P-P65）的表达和炎症变化。采用血红素诱导PC12细胞损伤，

体外模拟ICH模型，检测PF4、P-P65及纹状体炎症变化。利用短发夹RNA（shRNA-PF4）敲低PC12细胞中PF4的表达来检测炎症因子的变化。结果显示，术后48小时，脑出血行为评分最低。ICH组纹状体中PF4和P-P65的表达量显着高于假手术组。ICH组白细胞介素(IL)-6和IL-1b的表达也有较大改善。抑制NF-kB表达后，PF4表达下降。总之，ICH增强PF4的表达，从而通过NF-kB信号通路诱导脑出血大鼠的炎症反应。减少PF4的表达可以减轻炎症反应。