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首页> 外文期刊>Journal of inflammation. >Effect of remote ischemic post-conditioning on systemic inflammatory response and survival rate in lipopolysaccharide-induced systemic inflammation model
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Effect of remote ischemic post-conditioning on systemic inflammatory response and survival rate in lipopolysaccharide-induced systemic inflammation model

机译:远程缺血后处理对脂多糖诱导的全身炎症模型中全身炎症反应和存活率的影响

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Background Remote ischemic preconditioning (RIPC) and postconditioning (RpostC) have protective effects on ischemia and reperfusion injury. The effects have been reported to activate heme oxygenase-1 (HO-1) and attenuate nuclear factor kappa B (NF-κB) and subsequently reduce systemic inflammation. Ischemic preconditioning prevented inflammatory responses by modulating HO-1 expression in endotoxic shock model. Therefore, we investigated whether RpostC could have protective effects on lipopolysaccharide (LPS)-induced systemic inflammation. Methods The LPS-induced sepsis mice received LPS (20 mg/kg) intraperitoneally. Remote ischemic conditioning was induced with three 10-min ischemia/10-min reperfusion cycles of the right hind limbs using tourniquet before LPS injection (RIPC) or after LPS injection (RpostC). The effects of RIPC and RpostC were examined for the survival rate, serum cytokines, NF-κB, HO-1 and liver pathology in the LPS injected mice. Results Survival rate within 120 hours significantly increased in the LPS injected and remote ischemic conditioned mice than in LPS only injected mice (60-65% vs 5%, respectively, p?
机译:背景远程缺血预处理(RIPC)和后处理(RpostC)对缺血和再灌注损伤具有保护作用。据报道,这种作用可激活血红素加氧酶-1(HO-1),减弱核因子κB(NF-κB),从而减轻全身性炎症。缺血预处理通过调节内毒素休克模型中的HO-1表达来预防炎症反应。因此,我们调查了RpostC是否对脂多糖(LPS)诱导的全身性炎症具有保护作用。方法LPS引起的脓毒症小鼠腹腔注射LPS(20 mg / kg)。在LPS注射之前(RIPC)或LPS注射之后(RpostC)使用止血带,通过右后肢的三个10分钟局部缺血/ 10分钟再灌注循环诱导远程局部缺血。在注射LPS的小鼠中检查了RIPC和RpostC对存活率,血清细胞因子,NF-κB,HO-1和肝病理的影响。结果与仅注射LPS的小鼠相比,注射LPS的小鼠和远程缺血适应的小鼠在120小时内的存活率显着增加(分别为60-65%对5%,p << 0.01)。仅注射LPS的小鼠的肿瘤坏死因子-α(TNF-α),白介素-1β(IL-1β)和白介素-6(IL-6)显着增加,但是,远程缺血调节抑制了这种变化(p < 0.05)。在注射LPS的小鼠和经RpostC处理的小鼠中,白介素10(IL-10)的水平明显高于仅注射LPS的小鼠(p≥0.014)。与仅注射LPS的小鼠相比,注射LPS的小鼠和局部缺血的条件小鼠的NF-κB活化显着减弱(p≤0.05),HO-1水平明显更高。与仅注射LPS的小鼠相比,在注射LPS的小鼠和局部缺血的条件小鼠中,嗜中性粒细胞的浸润显着减弱(p <0.05)。结论RpostC可减轻LPS诱导的全身性炎症小鼠的炎症反应并改善其存活结果。该机制可能是由修饰NF-κB介导的细胞因子表达引起的。

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