背景:SENP5在TBI背景下影响神经元再生和凋亡的潜在机制仍未被探索。方法:在本研究中,用划痕处理24小时的PC12细胞被视为TBI细胞模型。通过定量实时PCR(qRT-PCR)和蛋白质印迹测定来测量PC12细胞中SENP5的表达。细胞计数试剂盒8(CCK-8)和流式细胞术测定用于评估TBI细胞的活性。此外,我们评估了体内抑制SENP5对TBI大鼠海马组织神经功能缺损和细胞凋亡的影响。通过免疫沉淀(IP)和双荧光素酶测定证明了SENP5与NEDD4L/TCF3轴之间的关系。结果:TBI细胞建模后,已发现SENP5表达增加。此外,TBI模型导致细胞活力降低和细胞凋亡增加,这是通过抑制SENP5来挽救的。体内实验表明,SENP5抑制可以减轻TBI引起的大鼠脑损伤。具体来说,这种抑制导致较低的神经功能缺损评分,改善神经元形态和结构,神经元凋亡减少。此外,NEDD4L已被证明与转录因子TCF3的稳定性增强有关,进而促进SENP5的表达。结论:本研究表明,抑制SENP5可以减轻TBI后的脑损伤。NEDD4L/TCF3轴可调控SENP5的表达影响TBI的发展。然而,SENP5调控TBI下游靶点,重要机制有待进一步探讨。
UNASSIGNED: The underlying mechanism of SENP5 influences neuronal regeneration and apoptosis in the context of TBI remains largely unexplored.
UNASSIGNED: In the present study, PC12 cells treated with scratch for 24 h were regarded as a TBI cell model. The expression of SENP5 in PC12 cells was measured via Quantitative Real-Time PCR (qRT-PCR) and western blot assays. Cell Counting Kit 8 (CCK-8) and Flow cytometry assays were used to evaluate the activity of TBI cells. In addition, we assessed the effect of inhibiting SENP5 in vivo on neurological function deficits and apoptosis in the hippocampal tissues of TBI rats. The relationship between SENP5 and
NEDD4L/TCF3 axis was proved via immunoprecipitation (IP) and double luciferase assays.
UNASSIGNED: Following TBI cell modeling, an increase in SENP5 expression has been found. Moreover, TBI modeling resulted in reduced cell viability and increased apoptosis, which was rescue by inhibition of SENP5. In vivo experiments demonstrated that SENP5 inhibition could mitigate TBI-induced brain injury in rats. Specifically, this inhibition led to lower neurological impairment scores, improved neuronal morphology and structure, and decreased neuronal apoptosis. In addition,
NEDD4L has been proved to be relevant to the enhanced stability of the transcription factor TCF3, which in turn promoted the expression of SENP5.
UNASSIGNED: This study reveals that inhibiting SENP5 can alleviate brain injury following TBI.
NEDD4L/TCF3 axis can regulate the expression of SENP5 to affect the development of TBI. However, SENP5 regulates downstream targets of TBI and important mechanisms need to be further explored.