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Abstract：
BACKGROUND: Spinal cord injury (SCI) is a traumatic neurological disorder with limited therapeutic options. Tumor protein p53-inducible nuclear protein 2 (TP53INP2) is involved in the occurrence and development of various diseases, and it may play a role during SCI via affecting inflammation and neuronal apoptosis. This study investigated the associated roles and mechanisms of TP53INP2 in SCI.
METHODS: Mouse and lipopolysaccharide (LPS)-induced SCI BV-2 cell models were constructed to explore the role of TP53INP2 in SCI and the associated mechanisms. Histopathological evaluation of spinal cord tissue was detected by hematoxylin and eosin staining. The Basso, Beattie, and Bresnahan score was used to measure the motor function of the mice, while the spinal cord water content was used to assess spinal cord edema. The expression of TP53INP2 was measured using RT-qPCR. In addition, inflammatory factors in the spinal cord tissue of SCI mice and LPS-treated BV-2 cells were measured using enzyme-linked immunosorbent assay. Apoptosis and related protein expression levels were detected by flow cytometry and western blot analysis, respectively.
RESULTS: TP53INP2 levels increased in SCI mice and LPS-treated BV-2 cells. The results of in vivo and in vitro experiments showed that TP53INP2 knockdown inhibited the inflammatory response and neuronal apoptosis in mouse spinal cord tissue or LPS-induced BV-2 cells.
CONCLUSIONS: After spinal cord injury, TP53INP2 was upregulated, and TP53INP2 knockdown inhibited the inflammatory response and apoptosis.
METHODS: Mouse and lipopolysaccharide (LPS)-induced SCI BV-2 cell models were constructed to explore the role of TP53INP2 in SCI and the associated mechanisms. Histopathological evaluation of spinal cord tissue was detected by hematoxylin and eosin staining. The Basso, Beattie, and Bresnahan score was used to measure the motor function of the mice, while the spinal cord water content was used to assess spinal cord edema. The expression of TP53INP2 was measured using RT-qPCR. In addition, inflammatory factors in the spinal cord tissue of SCI mice and LPS-treated BV-2 cells were measured using enzyme-linked immunosorbent assay. Apoptosis and related protein expression levels were detected by flow cytometry and western blot analysis, respectively.
RESULTS: TP53INP2 levels increased in SCI mice and LPS-treated BV-2 cells. The results of in vivo and in vitro experiments showed that TP53INP2 knockdown inhibited the inflammatory response and neuronal apoptosis in mouse spinal cord tissue or LPS-induced BV-2 cells.
CONCLUSIONS: After spinal cord injury, TP53INP2 was upregulated, and TP53INP2 knockdown inhibited the inflammatory response and apoptosis.
摘要：
背景：脊髓损伤（SCI）是一种治疗选择有限的创伤性神经系统疾病。肿瘤蛋白p53诱导核蛋白2(TP53INP2)参与多种疾病的发生发展,它可能在SCI过程中通过影响炎症和神经元凋亡发挥作用。本研究探讨了TP53INP2在SCI中的相关作用和机制。
方法：构建小鼠和脂多糖（LPS）诱导的SCIBV-2细胞模型，探讨TP53INP2在SCI中的作用及相关机制。通过苏木精和伊红染色检测脊髓组织的组织病理学评估。巴索,Beattie,Bresnahan评分用于测量小鼠的运动功能，而脊髓水含量用于评估脊髓水肿。使用RT-qPCR测量TP53INP2的表达。此外,采用酶联免疫吸附法检测SCI小鼠脊髓组织和LPS处理的BV-2细胞中的炎症因子。流式细胞术和Westernblot分析检测细胞凋亡及相关蛋白表达水平,分别。
结果：TP53INP2水平在SCI小鼠和LPS处理的BV-2细胞中增加。体内和体外实验结果表明，TP53INP2敲低抑制小鼠脊髓组织或LPS诱导的BV-2细胞的炎症反应和神经元凋亡。
结论：脊髓损伤后，TP53INP2上调,TP53INP2敲除抑制炎症反应和细胞凋亡。
方法：构建小鼠和脂多糖（LPS）诱导的SCIBV-2细胞模型，探讨TP53INP2在SCI中的作用及相关机制。通过苏木精和伊红染色检测脊髓组织的组织病理学评估。巴索,Beattie,Bresnahan评分用于测量小鼠的运动功能，而脊髓水含量用于评估脊髓水肿。使用RT-qPCR测量TP53INP2的表达。此外,采用酶联免疫吸附法检测SCI小鼠脊髓组织和LPS处理的BV-2细胞中的炎症因子。流式细胞术和Westernblot分析检测细胞凋亡及相关蛋白表达水平,分别。
结果：TP53INP2水平在SCI小鼠和LPS处理的BV-2细胞中增加。体内和体外实验结果表明，TP53INP2敲低抑制小鼠脊髓组织或LPS诱导的BV-2细胞的炎症反应和神经元凋亡。
结论：脊髓损伤后，TP53INP2上调,TP53INP2敲除抑制炎症反应和细胞凋亡。
