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目的采用NF-κB特异性抑制剂PDTC,观察NF-κB在MT保护LPS急性肝脏损伤中保护效应的作用机理。方法 MT+/+小鼠和MT-/-小鼠各分为4组,在注射LPS前30 min,腹腔注射PDTC 40 mg/kg,LPS剂量为10 mg/kg,24 h后处死动物。结果 PDTC预处理可以降低两种小鼠血清酶ALT、AST活性,减少血液中TNF-α、IL-1β、IL-6等细胞因子,血清以及肝脏组织中NO含量,降低肝组织TNF-α表达量,同时减轻两种小鼠肝脏组织病理学损伤程度,减轻肝组织内脂质过氧化产物生成量。以PDTC预处理消除MT自由基清除作用对NF-κB转录活性的影响后,不能观察到两种小鼠NF-κB转录活性间的差异,其未见两种小鼠肝脏损伤程度的差异。结论 MT可能通过其自由基清除作用调控NF-κB信号通路,从而影响整个炎症反应网络,造成了LPS致两种小鼠肝脏炎症损伤程度间的差异。
OBJECTIVE: To investigate the protective effect of NF-κB in the protection of acute liver injury induced by LPS by using NF-κB specific inhibitor PDTC. Methods MT + / + mice and MT - / - mice were divided into 4 groups. PDTC 40 mg / kg and LPS 10 mg / kg were injected intraperitoneally 30 minutes before LPS injection. Animals were killed 24 hours later. Results PDTC preconditioning could reduce the activity of ALT and AST, decrease the contents of TNF-α, IL-1β, IL-6 and other cytokines, serum and liver tissue, and decrease the expression of TNF-α in liver tissue While reducing the degree of histopathological damage in both liver tissues and reducing the production of lipid peroxidation products in liver tissue. PDTC pretreatment can eliminate the effect of MT free radical scavenging on the NF-κB transcriptional activity, and no difference in NF-κB transcriptional activity between the two mice was observed. There was no difference in liver damage between the two groups. Conclusion MT may regulate the NF-κB signaling pathway through its free radical scavenging effect, which may affect the whole inflammatory response network and cause the difference between the liver damage induced by LPS and the liver inflammation.