临床研究2025，Vol.33Issue(5)：5-9,5.DOI:10.12385/j.issn.2096-1278(2025)05-0005-05
利多卡因对脓毒症相关性脑病细胞模型的影响及机制
The Effect and Mechanism of Lidocaine on a Sepsis-Associated Encephalopathy Cell Model
摘要
Abstract
Objective To investigate the effects of lidocaine on a sepsis-associated encephalopathy cell model and the underlying mechanisms.Methods Neonatal SD rats within three days of birth were selected to isolate astrocytes from the cerebral cortex.The cells were then cultured using different culture media.The control group(Sham group)was cultured using high-glucose DMEM alone,while the sepsis-associated encephalopathy group(SAE group)was cultured with high-glucose DMEM supplemented with lipopolysaccharide(LPS).The sepsis-associated encephalopathy lidocaine intervention group(SAE+LD group)was cultured with high-glucose DMEM containing both LPS and lidocaine(LD).The culture duration was 48 hours.The levels of interleukin 6(IL-6)and tumor necrosis factor α(TNF-α)in the cell culture supernatant were measured using the ELISA method.The expression levels of high mobility group box 1(HMGB1),nuclear factor-κB(NF-κB),and Toll-like receptor 4(TLR4)were detected using Western Blot analysis,while HMGB1,TLR4,and NF-κB expression were assessed using immunofluorescence.Flow cytometry was used to detect cell apoptosis.Results Compared to the Sham group,the concentrations of IL-6 and TNF-α in the culture supernatants of the SAE and SAE+LD groups were significantly increased,with a statistically significant difference(P＜0.05).Compared to the SAE group,the concentrations of IL-6 and TNF-α in the SAE+LD group were significantly decreased,with a statistically significant difference(P＜0.05).Compared to the Sham group,the expression levels of HMGB1,TLR4,and NF-κB in the SAE and SAE+LD groups were significantly increased,with a statistically significant difference(P＜0.05).Compared to the SAE group,the expression levels of HMGB1,TLR4,and NF-κB in the SAE+LD group were significantly decreased,with a statistically significant difference(P＜0.05).Conclusion Lidocaine may exert anti-inflammatory effects by inhibiting HMGB1 protein,and the specific mechanism may be related to the suppression of HMGB1 translocation in astrocytes.关键词
脓毒症相关性脑病/利多卡因/星形胶质细胞/炎症介质/信号通路Key words
Sepsis-associated encephalopathy/Lidocaine/Astrocytes/Inflammatory mediators/Signaling pathways分类
医药卫生引用本文复制引用
张宇轩,刘一丹,马琳,李瑞轩,闫强,徐桂萍..利多卡因对脓毒症相关性脑病细胞模型的影响及机制[J].临床研究,2025,33(5):5-9,5.基金项目
自治区研究生创新项目(XJ2023G203). （XJ2023G203）
