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首页> 外文期刊>Journal of International Medical Research >Post-treatment curcumin reduced ischemia–reperfusion-induced pulmonary injury via the Notch2/Hes-1 pathway
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Post-treatment curcumin reduced ischemia–reperfusion-induced pulmonary injury via the Notch2/Hes-1 pathway

机译:治疗后姜黄素通过Notch2 / HES-1途径降低缺血再灌注诱导的肺损伤

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摘要

Objective To investigate the influence of curcumin on the Notch2/Hes-1 pathway after pulmonary injury induction via limb ischemia–reperfusion (I/R). Methods Adult male Sprague–Dawley rats were randomly divided into four groups (n?=?30 each): sham, I/R, curcumin post-treatment (I/R+Cur), and inhibitor (I/R+DAPT). Hind-limb ischemia was induced for 4 hours, followed by reperfusion for 4 hours. After ischemia, curcumin (200?mg/kg) or DAPT (0.5?μm) was injected intraperitoneally in the I/R+Cur or I/R+DAPT group, respectively. PaO _(2) was examined after 4 hours of reperfusion. Pathological changes in the lung and the apoptotic index (AI) were examined. Lung malondialdehyde (MDA), tumor necrosis factor (TNF)-α, and interleukin (IL)-1β levels, the wet/dry (W/D) ratio, semi-quantitative score of lung injury (SSLI), and Notch2 protein and Hes-1 mRNA expression were also examined. Results In the I/R group, inflammatory changes were observed, AI increased, and MDA, SSLI, W/D, TNF-α, IL-1β, Notch2, and Hes1-mRNA expression increased, while PaO _(2) decreased compared with the Sham group. Pathological changes in the I/R+Cur group were reversed. All indexes in the I/R+DAPT and I/R+Cur group were similar. Conclusion Curcumin post-treatment reduced I/R-induced lung injury in rats. Its mechanism may be related to the inhibition of Notch2/Hes-1 signaling pathway and the release of inflammatory factors.
机译:目的探讨姜黄素对肺部损伤诱导术后Notch2 / HES-1途径的影响(I / R)。方法将成年雄性Sprague-Dawley大鼠随机分为四组(n?=Δ30):假,I / R,姜黄素后处理(I / R + Cur)和抑制剂(I / R + DAPT)。诱导后肢缺血4小时,然后再灌注4小时。在缺血后,分别在I / R + Cur或I / R + DAPT组中腹膜内注射姜黄素(200→Mg / kg)或DAPT(0.5≤μm)。在再灌注4小时后检查PAO _(2)。检查了肺部和凋亡指数(AI)的病理变化。肺丙二醛(MDA),肿瘤坏死因子(TNF)-α和白细胞介素(IL)-1β水平,湿/干(w / d)比,肺损伤的半定量评分(ssli)和notch2蛋白还检查了HES-1 mRNA表达。结果在I / R组中,观察到炎症变化,AI增加,MDA,SSLI,W / D,TNF-α,IL-1β,NOTCH2和HES1-mRNA表达增加,而PAO_(2)相比减少与假小组。 I / R + Cur组的病理变化逆转。 I / R + DAPT和I / R + CUR组中的所有索引都是相似的。结论姜黄素后处理降低了大鼠I / R诱导的肺损伤。其机制可能与抑制Notch2 / HES-1信号通路和炎症因子的释放有关。

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