Liao Hai-Yang, Ran Rui, Da Chao-Ming, Wang Zhi-Qiang, Zhou Kai-Sheng, Zhang Hai-Hong
The Second Clinical Medical College of Lanzhou University, Lanzhou 730000, PR China; Department of Orthopaedics, Lanzhou University Second Hospital, Lanzhou 730000, PR China.
The Second Clinical Medical College of Lanzhou University, Lanzhou 730000, PR China; Department of Orthopaedics, Lanzhou University Second Hospital, Lanzhou 730000, PR China; Gansu Provincial Maternal and Child Health Hospital, 143 Qilihe North Street, Lanzhou 730050, PR China.
Neuroscience. 2022 May 10;490:250-263. doi: 10.1016/j.neuroscience.2022.02.015. Epub 2022 Mar 23.
Spinal cord injury (SCI) is a common disease of the nervous system, including primary and secondary injuries. Neuronal inflammation after SCI is the most important pathological process of SCI and a chemical barrier to nerve function recovery after injury. Ski, an evolutionarily conserved functional transcriptional regulator protein, is upregulated in reactive astrocytes after SCI and regulates the biological characteristics of astrocytes. However, its role in the glial inflammatory response triggered by reactive astrocytes after spinal cord ischemia and its exact mechanism remains unclear. This study investigated the role and mechanism of Ski in the inflammatory response triggered by reactive astrocytes induced by oxygen and sugar deprivation/reoxygenation (OGD/R) model in vitro. In the ODG/R model, Ski expression was upregulated. In contrast, Ski upregulation was accompanied by increased levels of iNOS, IL-1β, IL-6, TNF-α, and other inflammation-related factors. These results indicated that the inflammatory response triggered by astrocytes was significantly enhanced in OGD/R-stimulated astrocytes. Astrocytes were transfected with Ski specific siRNA to knock out Ski and subsequently attenuate OGD-induced astrocyte-triggered inflammation. Our results also suggest that Ski downregulation downregulates the expression of iNOS, IL-1β, IL-6, and TNF-α in OGD/R-induced reactive astrocytes by inhibiting the activity of the NF-κB signaling pathway. In conclusion, downregulation of Ski can effectively inhibit glial inflammation in SCI by inhibiting the activity of the NF-κB pathway. These findings suggest that Ski is a promising therapeutic target for inflammatory responses after SCI.In conclusion, Ski downregulation can effectively inhibit glial inflammation in SCI by inhibiting the activity of the NF-κB pathway. These findings suggest that Ski might serve as a promising target for the treatment of inflammatory responses after SCI.
脊髓损伤(SCI)是一种常见的神经系统疾病,包括原发性和继发性损伤。SCI后的神经元炎症是SCI最重要的病理过程,也是损伤后神经功能恢复的化学障碍。Ski是一种进化保守的功能性转录调节蛋白,在SCI后的反应性星形胶质细胞中上调,并调节星形胶质细胞的生物学特性。然而,其在脊髓缺血后反应性星形胶质细胞触发的胶质细胞炎症反应中的作用及其确切机制仍不清楚。本研究探讨了Ski在体外氧糖剥夺/复氧(OGD/R)模型诱导的反应性星形胶质细胞触发的炎症反应中的作用及机制。在OGD/R模型中,Ski表达上调。相反,Ski上调伴随着诱导型一氧化氮合酶(iNOS)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)等炎症相关因子水平的升高。这些结果表明,在OGD/R刺激的星形胶质细胞中,星形胶质细胞触发的炎症反应显著增强。用Ski特异性小干扰RNA(siRNA)转染星形胶质细胞以敲除Ski,随后减轻OGD诱导的星形胶质细胞触发的炎症。我们的结果还表明,Ski下调通过抑制核因子κB(NF-κB)信号通路的活性,下调OGD/R诱导的反应性星形胶质细胞中iNOS、IL-1β、IL-6和TNF-α的表达。总之,Ski下调可通过抑制NF-κB途径的活性有效抑制SCI中的胶质细胞炎症。这些发现表明,Ski是SCI后炎症反应的一个有前景的治疗靶点。总之,Ski下调可通过抑制NF-κB途径的活性有效抑制SCI中的胶质细胞炎症。这些发现表明,Ski可能是治疗SCI后炎症反应的一个有前景的靶点。