Gu Xiaoyu, Ni Haibo, Kan XuGang, Chen Chen, Zhou Zhiping, Ding Zheng, Li Di, Liu Bofei
Department of Intensive Care Unit, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
Department of Neurosurgery, The Affiliated Zhangjiagang Hospital of Soochow University, Suzhou, China.
J Korean Neurosurg Soc. 2023 Jul;66(4):400-408. doi: 10.3340/jkns.2022.0115. Epub 2022 Oct 27.
Nicotinamide mononucleotide adenylyl transferase 2 (NMNAT2) is a crucial factor for the survival of neuron. The role of NMNAT2 in damage following traumatic brain injury (TBI) remains unknown. This study was designed to investigate the role of NMNAT2 in TBI-induced neuronal degeneration and neurological deficits in rats.
The TBI model was established in Sprague-Dawley rats by a weight-dropping method. Real-time polymerase chain reaction, western blot, immunofluorescence, Fluoro-Jade C staining, and neurological score analyses were carried out.
NMNAT2 mRNA and protein levels were increased in the injured-side cortex at 6 hours and peaked 12 hours after TBI. Knocking down NMNAT2 with an injection of small interfering RNA in lateral ventricle significantly exacerbated neuronal degeneration and neurological deficits after TBI, which were accompanied by increased expression of BCL-2-associated X protein (Bax).
NMNAT2 expression is increased and NMNAT2 exhibits neuroprotective activity in the early stages after TBI, and Bax signaling pathway may be involved in the process. Thus, NMNAT2 is likely to be an important target to prevent secondary damage following TBI.
烟酰胺单核苷酸腺苷酸转移酶2（NMNAT2）是神经元存活的关键因素。NMNAT2在创伤性脑损伤（TBI）后的损伤中所起的作用尚不清楚。本研究旨在探讨NMNAT2在TBI诱导的大鼠神经元变性和神经功能缺损中的作用。
采用重物坠落法在Sprague-Dawley大鼠中建立TBI模型。进行实时聚合酶链反应、蛋白质免疫印迹、免疫荧光、荧光玉髓C染色和神经功能评分分析。
TBI后6小时，损伤侧皮质中NMNAT2 mRNA和蛋白水平升高，并在12小时达到峰值。在侧脑室内注射小干扰RNA敲低NMNAT2显著加剧了TBI后的神经元变性和神经功能缺损，同时伴有BCL-2相关X蛋白（Bax）表达增加。
TBI后早期NMNAT2表达增加，且NMNAT2具有神经保护活性，Bax信号通路可能参与了这一过程。因此，NMNAT2可能是预防TBI后继发性损伤的重要靶点。
