天津医药

天津医药 ›› 2021, Vol. 49 ›› Issue (6): 588-592.doi: 10.11958/20203007

• 实验研究 • 上一篇    下一篇

大黄素对肺炎链球菌肺炎大鼠氧化应激损伤及miR-34a/SIRT1轴的影响

张小红，王红民，李杨，胡朝阳，李凤芝，常瑞，黄晗，靳莉   

  1. 1郑州大学附属郑州中心医院呼吸与危重症医学科（邮编450000）；2郑州大学第一附属医院呼吸科

  • 收稿日期:2020-11-02 修回日期:2021-02-02 出版日期:2021-06-15 发布日期:2021-06-15
  • 通讯作者: 张小红 E-mail:hnxh70@163.com
  • 基金资助:
    2018年度河南省科技攻关项目

Effects of emodin on oxidative stress damage and miR-34a/SIRT1 axis in rat model of streptococcus pneumoniae pneumonia

ZHANG Xiao-hong, WANG Hong-min, LI Yang, HU Chao-yang, LI Feng-zhi, CHANG Rui, HUANG Han, JIN Li #br#   

  1. 1 Department of Respiratory and Critical Care Medicine, Zhengzhou Central Hospital Affiliated to Zhengzhou University,
    Zhengzhou 450000, China; 2 Department of Respiratory Medicine, the First Affiliated Hospital of Zhengzhou University
  • Received:2020-11-02 Revised:2021-02-02 Published:2021-06-15 Online:2021-06-15
  • Contact: Xiaohong ZHANG E-mail:hnxh70@163.com

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摘要： 目的 探究大黄素对肺炎链球菌肺炎大鼠氧化应激损伤及微小RNA-34a/沉默信息调节因子2相关酶1 （miR-34a/SIRT1）轴的影响。方法 60只雄性SD大鼠按照随机数字表法分为假手术组、模型组、低剂量（20 mg/kg）、 中剂量（40 mg/kg）和高剂量（80 mg/kg）大黄素组，每组12只。采用气管滴加肺炎链球菌法制备肺炎模型，建模成功 后24 h，大黄素干预组分别腹腔注射大黄素溶液，每天1次，连续7 d。HE染色观察肺组织病理变化，酶联免疫吸附 测定（ELISA）法检测肺组织肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）和谷胱甘肽过氧化物酶（GSH-Px）水平, 可见分光光度法检测超氧化物歧化酶（SOD）、丙二醛（MDA）水平，qPCR 检测肺组织 miR-34a、SIRT1 mRNA 水平， Western blot 检测肺组织SIRT1蛋白表达。结果 假手术组大鼠肺组织正常，无明显病理改变；模型组大鼠肺泡塌 陷，有大量炎性细胞浸润；低、中、高剂量大黄素组肺组织炎性病变均减轻。与假手术组比较，模型组肺组织TNF-α、 IL-6、MDA、miR-34a水平显著增加（P＜0.05），肺组织SOD、GSH-Px、SIRT1 mRNA及蛋白水平显著降低（P＜0.05）。 与模型组比较，中、高剂量大黄素组大鼠肺组织TNF-α、IL-6、MDA、miR-34a水平显著降低（P＜0.05），肺组织SOD、 GSH-Px及SIRT1 mRNA及蛋白水平显著增加（P＜0.05），其中高剂量大黄素组变化最明显。结论 大黄素可减轻肺 炎链球菌肺炎大鼠炎症反应及氧化应激损伤，可能与调控miR-34a/SIRT1轴有关。

关键词: 大黄素, 肺炎, 肺炎球菌性, 大鼠, Sprague-Dawley, 氧化性应激, 微小RNA-34a/沉默信息调节因子2相关酶1轴

Abstract: Objective To investigate the effects of emodin on oxidative stress injury and microRNA-34a/silent information regulator factor 2 related enzyme 1 (miR-34a/SIRT1) axis in streptococcus pneumoniae pneumonia rat model. Methods According to random number table, sixty rats were divided into sham operation group, model group, low-dose (20 mg/kg) emodin group, middle-dose (40 mg/kg) emodin group and high-dose (80 mg/kg) emodin group, with 12 rats in each group. The model of pneumonia was established by intratracheal instillation of streptococcus pneumoniae. At 24 h after successful modeling, the emodin intervention group was intraperitoneally injected with emodin solution once a day for 7 days. HE staining was used to detect the pathological changes of lung tissue. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and glutathione peroxidase (GSH-Px). UV-VIS spectrophotometer was used to detect the levels of superoxide dismutase (SOD) and malondialdehyde (MDA). The levels of miR-34a and SIRT1 mRNA in lung tissue were detected by qPCR. The expression of SIRT1 protein was detected by Western blot assay. Results In the sham operation group, the lung tissue was normal without obvious pathological changes. In the model group, it was found that the alveoli collapsed and a large number of inflammatory cells infiltrated. In the low, middle and high dose emodin groups, the inflammatory lesions of lung tissue were alleviated. Compared with those in the sham operation group, the levels of TNF-α, IL-6, MDA and miR-34a were significantly higher in the model group (P <0.05), and the levels of SOD, GSH-Px and SIRT1 mRNA and protein in lung tissue were significantly lower (P < 0.05). Compared with those in the model group, the levels of TNF- α, IL-6, MDA and miR-34a were significantly lower in the middle and high-dose emodin groups (P < 0.05), and the levels of SOD, GSH-Px and SIRT1 mRNA and protein in lung tissue were significantly higher (P < 0.05), in which the high-dose emodin group showed the most obvious changes. Conclusion Emodin can reduce inflammatory reaction and oxidative stress injury in rat model of streptococcus pneumoniae pneumonia, which may be related to the regulation of miR-34a/SIRT1 axis.

Key words: emodin, pneumonia, pneumococcal, rats, Sprague-Dawley, oxidative stress, microRNA-34a/silent information regulator factor 2 related enzyme 1 axis