高压氧调控TLR4/NF-κB通路对脓毒症大鼠海马区细胞凋亡的影响

doi:10.3969/j.issn.1006-6233.2022.01.01

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摘要 目的:探究高压氧(hyperbaric oxygenation,HBO)调控Toll样受体4(Toll-like receptor 4,TLR4)/核因子(nuclear factor,NF)-κB通路对脓毒症相关性脑病(sepsis-associated encephalopathy,SAE)大鼠海马区细胞凋亡的影响。方法:将45只大鼠随机分为对照组、SAE组和SAE+HBO组(n=15),腹腔注射LPS构建SAE模型(15mg/kg,3d),SAE+HBO组大鼠每日接受HBO干预。检测和比较各组脑神经功能、海马体神经元损伤、凋亡、炎性反应水平,评估海马体中TLR4和NF-κB转录和翻译水平。结果:三组大鼠上述各指标比较差异显著(P<0.05)。SAE组的逃避潜伏期(44.06±5.12s)、IL-1β(76.25±8.06pg/mL)、IL-6(91.37±10.74pg/mL)、海马神经元损伤和凋亡(6.17±0.78个/视野)、TLR4和NF-κB mRNA和蛋白水平显著高于对照组,穿越平台次数(2.94±0.35次)显著低于对照组(P<0.05)。SAE+HBO组的逃避潜伏期(35.86±3.06s)、IL-1β(48.68±5.21pg/mL)、IL-6(64.47±7.06pg/mL)、海马神经元损伤和凋亡(3.42±0.52个/视野)、TLR4和NF-κB mRNA和蛋白水平显著低于SAE组,穿越平台次数(4.98±0.66次)显著高于SAE组(P<0.05)。结论:HBO可能通过抑制TLR4/NF-κB通路缓解SAE引起的海马神经元损伤和凋亡,进而保护神经功能。

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	郭慧
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关键词 ：脓毒症, 脓毒症相关性脑病, 高压氧, Toll样受体4, 核因子-κB, 海马体

Abstract：Objective: To explore the effect of hyperbaric oxygen (HBO) on apoptosis in hippocampus of rats with sepsis-related encephalopathy (SAE) by regulating the Toll-like receptor 4 (TLR4)/nuclear factor (NF)-κB pathway. Methods: 45 rats were randomly divided into control group, SAE group and SAE+HBO group (n=15). The SAE model was constructed by intraperitoneal injection of LPS (15 mg/kg, 3 days). Rats in SAE+HBO group received HBO intervention daily. The cranial nerve function, hippocampal neuron damage, apoptosis, and inflammatory response levels in each group were tested and compared. TLR4 and NF-κB transcription and translation levels in the hippocampus were detected. Results: The above indicators of the three groups of rats were significantly different (P<0.05). The escape latency (44.06±5.12 s), IL-1β (76.25±8.06 pg/mL), IL-6 (91.37±10.74 pg/mL), hippocampal neuron damage and apoptosis (6.17±0.78 cells/field of view), TLR4 and NF-κB mRNA and protein levels in SAE group were significantly higher than those of the control group, and the number of crossing platforms (2.94±0.35 times) was significantly lower than that of the control group (P<0.05). The escape latency (35.86±3.06 s), IL-1β (48.68±5.21 pg/mL), IL-6 (64.47±7.06 pg/mL), hippocampal neuron damage and apoptosis (3.42±0.52 cells/field of view), TLR4 and NF-κB mRNA and protein levels in the SAE+HBO group were significantly lower than those in the SAE group, and the number of crossing platforms (4.98±0.66 times) was significantly higher than in the SAE group (P<0.05). Conclusion: HBO may alleviate the damage and apoptosis of hippocampal neurons caused by SAE by inhibiting the TLR4 /NF-κB pathway, thereby protecting nerve function.

Key words： Sepsis Sepsis-related encephalopathy Hyperbaric oxygen Toll-like receptor 4 Nuclear factor-κB Hippocampus

基金资助:河北省卫生和计划生育委员会科研基金项目,(编号:20170273)

通讯作者: 李建国

引用本文:

郭慧, 李旭蕊, 曲珍珍, 李建国. 高压氧调控TLR4/NF-κB通路对脓毒症大鼠海马区细胞凋亡的影响[J]. 河北医学, 2022, 28(1): 1-5.
GUO Hui, LI Xurui, QU Zhenzhen, et al. Effects of Hyperbaric Oxygen Regulation of TLR4/NF-κB Pathway on Apoptosis in Hippocampus of Septic Rats. HeBei Med, 2022, 28(1): 1-5.

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