Effect of remote ischemic post-conditioning on systemic inflammatory response and survival rate in lipopolysaccharide-induced systemic inflammation model.
Effect of remote ischemic post-conditioning on systemic inflammatory response and survival rate in lipopolysaccharide-induced systemic inflammation model.
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DOI：
10.1186/1476-9255-11-16
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发表时间：
2014
期刊：
影响因子：
--
通讯作者：
Lim CH
中科院分区：
文献类型：
--
作者：
Kim YH;Yoon DW;Kim JH;Lee JH;Lim CH
远程缺血预处理（RIPC）和后处理（RpostC）对缺血再灌注损伤具有保护作用。据报道，该作用可激活血红素加氧酶-1（HO-1）并减弱核因子κ B（NF-κB），随后减轻全身炎症。缺血预处理通过调节HO-1表达预防内毒素休克模型的炎症反应。因此，我们研究了RpostC是否可以对脂多糖（LPS）诱导的全身炎症具有保护作用。LPS诱导的脓毒症小鼠腹腔注射LPS（20 mg/kg）。在LPS注射前（RIPC）或LPS注射后（RpostC）使用止血带对右后肢进行3次10 min缺血/10 min再灌注循环诱导远程缺血条件反射。观察RIPC和RpostC对LPS注射小鼠存活率、血清细胞因子、NF-κB、HO-1和肝脏病理学的影响。与仅注射LPS的小鼠相比，注射LPS的小鼠和远端缺血条件小鼠在120小时内的存活率显著增加（分别为60-65%对5%，p < 0.01）。单纯LPS注射组肿瘤坏死因子-α（TNF-α）、白细胞介素-1 β（IL-1β）和白细胞介素-6（IL-6）均显著升高，而远程缺血处理抑制了这些变化（p < 0.05）。注射LPS和RpostC处理的小鼠中的白细胞介素-10（IL-10）水平显著高于仅注射LPS的小鼠（p = 0.014）。NF-κB活化显著减弱（p < 0.05），HO-1水平在LPS注射和远程缺血条件小鼠中显著高于仅注射LPS的小鼠。与单纯LPS注射组相比，LPS注射组和远端缺血组的神经细胞浸润明显减少（p < 0.05）。RpostC减弱了炎症反应，改善了LPS诱导的全身炎症小鼠的生存结果。其机制可能与调节NF-κB介导的细胞因子表达有关。
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. 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. 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 < 0.01). Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) increased markedly in the LPS only injected mice, however, remote ischemic conditioning suppressed the changes (p < 0.05). Interleukin-10 (IL-10) level was significantly higher in the LPS injected and RpostC treated mice than in the LPS only injected mice (p = 0.014). NF-κB activation was significantly attenuated (p < 0.05) and HO-1 levels were substantially higher in the LPS injected and remote ischemic conditioned mice than in the LPS only injected mice. Neutrophil infiltration was significantly attenuated in the LPS injected and remote ischemic conditioned mice than in the only LPS injected mice (p < 0.05). RpostC attenuated inflammatory responses and improved survival outcomes of mice with LPS-induced systemic inflammation. The mechanism may be caused by modifying NF-κB mediated expression of cytokines.
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影响因子：
8.8
作者：
DEBETS, JMH;KAMPMEIJER, R;VANDERLINDEN, CJ
通讯作者：
VANDERLINDEN, CJ
影响因子：
5.6
作者：
Bellezza, Ilaria;Tucci, Arianna;Minelli, Alba
通讯作者：
Minelli, Alba
影响因子：
6.4
作者：
Gibbs, Peter E. M.;Maines, Mahin D.
通讯作者：
Maines, Mahin D.
DOI：
10.1097/00005373-199904000-00006
发表时间：
1999-04-01
影响因子：
--
作者：
Browder, W;Ha, TZ;Williams, DL
通讯作者：
Williams, DL
影响因子：
6.2
作者：
Lai, I-Rue;Chang, King-Jen;Tsai, Hsiu-Wen
通讯作者：
Tsai, Hsiu-Wen