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王 茜.黄芪甲苷介导 TLR4-p38 MAPK 信号通路在幼鼠 急性肺损伤中的研究[J].中国比较医学杂志,2020,30(6):106~112.
黄芪甲苷介导 TLR4-p38 MAPK 信号通路在幼鼠 急性肺损伤中的研究
Astragaloside inhibits the TLR4-p38 MAPK signaling pathway in acute lung injury in newborn mice
投稿时间:2019-12-19  
DOI:10. 3969 / j.issn.1671-7856. 2020. 06. 016
中文关键词:  黄芪甲苷  急性肺损伤模型  TLR4-p38 MAPKs 信号通路  炎症因子
英文关键词:astragaloside  acute lung injury model  TLR4-p38 MAPK signaling pathway  inflammatory factors
基金项目:
作者单位E-mail
王 茜 华中科技大学同济医学院附属武汉中心医院儿科,武汉 430014 439547611@ qq.com 
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中文摘要:
      目的 探究黄芪甲苷介导 TLR4-p38 MAPK 信号通路在幼鼠急性肺损伤模型中的作用。 方法 以 7 日龄 SD 新生仔鼠为实验对象,利用脂多糖构建幼鼠急性肺损伤模型,以地塞米松为阳性药对照,每只幼鼠腹腔注 射 10 mL/ kg 黄芪甲苷,造模后 12 h 和 24 h 观察肺组织病变,检测 TLR4、p-p38 蛋白和 mRNA 表达量,TNF-α、IL-6、 IL-12 炎症因子的 mRNA 表达量变化。 结果 模型组在建模后 12 h 呈现肺出血,大量肺泡萎陷,24 h 呈现肺水肿, 肺泡间隔明显增宽。 和模型组相比,黄芪甲苷组肺组织的病变明显减轻。 另外,蛋白检测结果表明,与模型组比 较,黄芪甲苷组 TLR4、p-p38 蛋白表达量明显降低(P< 0. 05,P< 0. 001)q-PCR 结果表明,与模型组比较,黄芪甲苷组 TLR4 mRNA 相对表达量均有明显的降低,并且和模型组有显著性差异(P< 0. 05)。 TNF-α、IL-6、IL-12 各炎症因子 均有下降的趋势,其中 IL-12 相对表达量和模型组有显著性差异(P< 0. 05)。 结论 黄芪甲苷通过抑制 TLR4-p38 MAPK 信号通路,在幼鼠急性肺损伤模型中起重要作用。
英文摘要:
      Objective To investigate the effect of astragaloside on the TLR4-p38 MAPK signaling pathway in a newborn mouse acute lung injury model. Methods Seven-day-old SD newborn rats were used as experimental subjects. The model of acute lung injury in newborn rats was established by intraperitoneal lipopolysaccharide ( LPS) injection. Dexamethasone was used as a positive control. Each rat was injected intraperitoneally with 10 mL/ kg astragaloside. The lung lesions were observed 12 and 24 h after LPS injection. Furthermore, the mRNA and protein expression levels of TLR4 were determined, as well as the phosphorylation level of p38 protein. Finally, the changes in inflammatory factors TNF-α, IL-6 and IL-12 were analyzed. Results The model group showed pulmonary hemorrhage and a large number of collapsed alveoli at 12 h, and pulmonary edema and a significantly widened alveolar septum at 24 h after LPS injection. Compared with the model group, the lesions in the lung tissue of the astragaloside group were significantly alleviated. Additionally, Western blot result showed the levels of TLR4 (P< 0. 05) and p-p38 (P< 0. 001) were significantly lower in the astragaloside group than in the model group. The qPCR result showed that the level of TLR4 mRNA in the astragaloside group was significantly decreased compared with that in the model group (P< 0. 05). The inflammatory factors, TNF-α, IL-6 and IL- 12, were all decreased, and the relative IL-12 expression was significantly different from that in the model group (P< 0. 05). Conclusions Astragaloside plays an important role in alleviating the acute lung injury model of newborn rats by inhibiting the TLR4-p38 MAPK signaling pathway.
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