陕西医学杂志2024，Vol.53Issue(1)：23-27,5.DOI:10.3969/j.issn.1000-7377.2024.01.005
右美托咪定通过沉默信息调节因子1/核转录因子信号通路调控脑梗死大鼠海马组织炎症机制研究
Mechanism of dexmedetomidine regulating hippocampal inflammation in rats with cerebral infarction through SIRT1/NF-κB signaling pathway
摘要
Abstract
Objective:To investigate the therapeutic effect of dexmedetomidine(Dex)intervention on cerebral infarction in rats and its potential therapeutic mechanism.Methods:A total of 60 SPF male SD rats were randomly di-vided into control group,sham operation group,model group,low-dose Dex group and high-dose Dex group,with 12 rats in each group.The middle cerebral artery occlusion(MCAO)model was prepared by Longa suture method in the other groups except the control group and the sham operation group.Only the muscle vessels were stripped in the sham operation group.The Dex treatment group was intraperitoneally injected with dexmedetomidine hydrochloride solution,and the other groups were treated with the same amount of 0.9％sodium chloride solution.The mRNA and protein expression levels of silent information regulator 1(SIRT1)and nuclear factor-κb(NK-κB)and the levels of malondialdehyde(MDA)and superoxide dismutase(SOD)in ischemic brain tissue were compared among the groups.The levels of inflammatory factors tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in the hippo-campus of rats in each group were detected,and the levels of inflammatory factors TNF-α and IL-6 in the hippocam-pus of rats in each group were detected.Results:Compared with the control group,the mRNA and protein levels of SIRT1 were decreased and the mRNA and protein levels of NF-KB were increased in the DEX-treated group.After Dex treatment,the mRNA and protein levels of SIRT1 were increased in the two groups,and the high-dose Dex group had a higher expression.At the same time,the NF-κB mRNA and protein levels decreased,and high-dose Dex group was lower than the low-dose Dex group.Compared with the control group and the sham-operation group,the levels of TNF-α,IL-6 and MDA in the other groups were increased,and the level of SOD was decreased.After Dex treatment,the inflammatory factors and oxidative stress levels in the two groups were decreased,and the levels of TNF-α,IL-6 and MDA in the high-dose Dex group were lower than those in the low-dose Dex group,and the level of SOD was increased,and the high-dose Dex group was higher(all P＜0.05).Conclusion:Dexmedetomidine may allevi-ate inflammatory response and oxidative stress by activating SIRT1/NF-kB signaling pathway to exert brain protection.关键词
右美托咪定/沉默信息调节因子1/核转录因子/肿瘤坏死因子-α/白细胞介素-6/氧化应激/机制Key words
Dexmedetomidine/Silent information regulator 1/nuclear factor/TNF-α/IL-6/Oxidative stress/Mechanism分类
医药卫生引用本文复制引用
李显碧,刘尚升,肖兵,廖华,张杨..右美托咪定通过沉默信息调节因子1/核转录因子信号通路调控脑梗死大鼠海马组织炎症机制研究[J].陕西医学杂志,2024,53(1):23-27,5.基金项目
四川省医学会科研项目(2021XHNJ36) （2021XHNJ36）
