七氟醚(SEV),通常会导致神经元损伤和认知功能障碍,是临床上最常用的麻醉药之一。然而,Trim47在SEV诱导的神经元损伤中的功能仍然难以捉摸。本研究的目的是研究敲除Trim47对SEV引起的神经损伤的影响。3%SEV诱导大鼠神经损伤,用H19-7建立病理模型,然后将sh-Trim47转染到H19-7中以研究Trim47的功能。通过神经功能评分和Moris水迷宫(MWM)研究SEV对大鼠海马Trim47表达及认知功能的影响。TNF-α的mRNA和蛋白表达,细胞中的IL-1β和IL-6,通过TUNEL或WB研究各组大鼠海马神经元凋亡。流式细胞术用于研究敲低Trim47对细胞凋亡的影响。CCK-8用于检测H19-7细胞的细胞活力。最后,通过WB研究SEV诱导后Trim47敲低对潜在信号通路的影响。结果表明,敲除Trim47改善SEV引起的神经损伤和认知缺陷,大鼠炎症和神经细胞凋亡,并促进海马神经元活动。敲除Trim47抑制NF-κB信号通路,通过调节NF-κB信号通路改善SEV诱导的新生大鼠神经细胞损伤和认知障碍,缓解炎症反应,并抑制神经元凋亡。
Sevoflurane (SEV), usually causing neuronal damage and cognitive dysfunction, is one of the most commonly used anesthetics in clinical practice. However, the function of
Trim47 in SEV-induced neuronal impairment remains elusive. The aim of this study was to study the effect of knocking down
Trim47 on the nerve injury induced by SEV. Nerve injury was induced in rats by 3% SEV, and H19-7 was used to establish a pathological model, and sh-Trim47 was transfected into H19-7 to study the function of
Trim47. The effects of SEV on the expression of
Trim47 in the hippocampus and cognitive function of rats were studied by neurological function score and Moris water maze (MWM). The mRNA and protein expression of TNF-α, IL-1β and IL-6 in the cells, along with the neuronal apoptosis in the hippocampus of rats in each group were studied by TUNEL or WB. Flow cytometry was used to study the effect of knockdown of
Trim47 on cell apoptosis. CCK-8 was used to detect cell viability of H19-7 cells. Finally, the potential signaling pathway affected by knockdown of Trim47 after abrogation of SEV induction was investigated by WB. The results showed that, knockdown of Trim47 ameliorated SEV-induced neurological damage and cognitive deficits, inflammation and neuronal cell apoptosis in rats, and promoted hippocampal neuronal activity. Knockdown of Trim47 can inhibit the NF-κB signaling pathway and improve neuronal cell damage and cognitive impairment induced by SEV in neonatal rats by regulating NF-κB signaling pathway, alleviating inflammatory response, and inhibiting neuronal apoptosis.