本文選題：脂多糖類(lèi) + 膿毒癥��； 參考：《軍事醫(yī)學(xué)》2016年09期

【摘要】：目的探討脂多糖(lipopolysaccharide,LPS)誘導(dǎo)的膿毒癥造成大鼠腦內(nèi)氧化損傷的作用及JNK、Nrf2相關(guān)信號(hào)的變化。方法將大鼠隨機(jī)分為對(duì)照組、低劑量模型組(LPS 5 mg/kg)和高劑量模型組(LPS 10 mg/kg)。模型組造模24 h后,活殺大鼠,將腦組織完全取出后,剪碎并研磨成腦勻漿,檢測(cè)丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽過(guò)氧化物酶(GSH-Px)、總抗氧化能力(T-AOC)、過(guò)氧化氫(H2O2)、琥珀酸脫氫酶(SDH)的變化。利用qRT-PCR、Western印跡檢測(cè)JNK與Nrf2蛋白在腦組織亞細(xì)胞中的表達(dá)水平。結(jié)果與對(duì)照組比較,在LPS誘導(dǎo)膿毒癥大鼠模型中,模型組大鼠腦組織中,MDA、H2O2、SDH含量增加,SOD、GSH-Px、T-AOC含量減少,JNK mRNA水平與總蛋白水平未受明顯影響(P0.05),但磷酸化水平(p-JNK)顯著升高(P0.01);Nrf2 mRNA水平與總蛋白水平顯著上調(diào)(P0.01),且磷酸化水平(p-Nrf2)也顯著升高(P0.01),差異具有統(tǒng)計(jì)學(xué)意義。結(jié)論成功構(gòu)建LPS誘導(dǎo)膿毒血癥后大鼠腦內(nèi)氧化損傷的病理模型,并發(fā)現(xiàn)在這一病理過(guò)程中p-JNK、總Nrf2以及p-Nrf2表達(dá)顯著上調(diào),提示JNK、Nrf2相關(guān)通路在LPS誘導(dǎo)膿毒癥腦損傷中可能參與重要的介導(dǎo)作用。
[Abstract]:Objective to investigate the effects of lipopolysaccharide (LPS) -induced sepsis on oxidative damage in rat brain and the changes of JNK-Nrf2 related signals. Methods Rats were randomly divided into control group, low dose model group (LP5 mg/kg) and high dose model group (LPS-10 mg/kg). In the model group, after 24 hours of modeling, the rats were killed alive, the brain tissue was completely removed, and the brain homogenate was cut and ground into a brain homogenate. Malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), hydrogen peroxide (H2O2) and succinate dehydrogenase (SDH) were measured. The expression of JNK and Nrf2 proteins in brain subcells was detected by qRT-PCR- Western blot. Results compared with the control group, in LPS induced sepsis rat model, In the model group, the content of SDH in the brain tissue of MDA-H _ 2O _ 2 increased and the content of GSH-PxX T-AOC decreased significantly (P0.05), but the level of phosphorylation (p-JNK) increased significantly (P0.01), and the level of phosphorylation (p-Nrf2) also increased significantly (P0.01), and the level of phosphorylation (p-Nrf2) was also significantly increased (P0.01), while the level of phosphorylation (p-Nrf2) was also significantly increased (P0.01), while the level of phosphorylation (p-Nrf2) was also significantly increased (P0.01). The difference was statistically significant (P0.01). Conclusion the pathological model of oxidative injury induced by LPS in rats with sepsis was successfully constructed, and it was found that the expression of p-JNK2, total Nrf2 and p-Nrf2 were significantly up-regulated during the pathological process. These results suggest that JNKN Nrf2 pathway may play an important role in LPS induced septic brain injury.
【作者單位】： 天津醫(yī)科大學(xué)研究生院;武警后勤學(xué)院附屬醫(yī)院救援醫(yī)學(xué)研究所;
【基金】：天津市科技計(jì)劃資助項(xiàng)目(14ZCDZSY00033) 天津市應(yīng)用基礎(chǔ)與前沿技術(shù)研究計(jì)劃資助項(xiàng)目(14JCQNJC12600) 全軍重點(diǎn)實(shí)驗(yàn)室開(kāi)放基金資助項(xiàng)目(JY1402)
【分類(lèi)號(hào)】：R459.7

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