张小利, 李波, 邵蔚, 沈彤, 章静. 甘草酸单糖对单壁碳纳米管暴露小鼠急性肺损伤的保护作用研究[J]. 职业卫生与应急救援, 2023, 41(2): 220-223. DOI: 10.16369/j.oher.issn.1007-1326.2023.02.021
引用本文: 张小利, 李波, 邵蔚, 沈彤, 章静. 甘草酸单糖对单壁碳纳米管暴露小鼠急性肺损伤的保护作用研究[J]. 职业卫生与应急救援, 2023, 41(2): 220-223. DOI: 10.16369/j.oher.issn.1007-1326.2023.02.021
ZHANG Xiaoli, LI Bo, SHAO Wei, SHEN Tong, ZHANG Jing. Protective effect of glycyrrhizic acid monosaccharide on acute lung injury caused by single-walled carbon nanotubes in mice[J]. Occupational Health and Emergency Rescue, 2023, 41(2): 220-223. DOI: 10.16369/j.oher.issn.1007-1326.2023.02.021
Citation: ZHANG Xiaoli, LI Bo, SHAO Wei, SHEN Tong, ZHANG Jing. Protective effect of glycyrrhizic acid monosaccharide on acute lung injury caused by single-walled carbon nanotubes in mice[J]. Occupational Health and Emergency Rescue, 2023, 41(2): 220-223. DOI: 10.16369/j.oher.issn.1007-1326.2023.02.021

甘草酸单糖对单壁碳纳米管暴露小鼠急性肺损伤的保护作用研究

Protective effect of glycyrrhizic acid monosaccharide on acute lung injury caused by single-walled carbon nanotubes in mice

  • 摘要:
      目的  评估甘草酸单糖(glycyrrhizic acid monoglucuronide,GAMG)对单壁碳纳米管(single-walled carbon nanotubes,SWCNT)诱导的小鼠急性肺损伤的保护作用。
      方法  取7 ~ 8周龄雌性C57/BL小鼠30只,随机分为3组,每组10只,分别为阴性对照组(生理盐水40 μg/只,气管滴注)、SWCNT模型组(SWCNT 40 μg/只,气管滴注)、GAMG治疗组(SWCNT 40 μg/只,气管滴注+ GAMG 200 mg/kg),GAMG治疗组每天给予1次GAMG腹腔注射,连续3 d,其他组同时给予空白溶剂,在第3天对小鼠进行取材。观察各组小鼠肺组织HE染色病理改变和气管肺泡灌洗液中细胞因子白介素-6(IL-6)和单核细胞趋化蛋白1(MCP-1)的变化,采用免疫组化法检测TLR4/MyD88/NF-κB信号通路的蛋白表达水平,免疫荧光法检测NF-κB和HSP47的含量。
      结果  GAMG治疗组小鼠肺损伤程度明显减轻。与SWCNT组相比,GAMG治疗组BALF中MCP-1和IL-6水平降低(P < 0.01);TLR4和MyD88的表达减少,肺组织NF-κB p65和HSP47蛋白表达减少(P < 0.01)。
      结论  GAMG可显著改善SWCNT诱导的急性肺损伤,并抑制肺内TLR4/MyD88/NF-κB信号通路的激活。

     

    Abstract:
      Objective  To evaluate the protective effect of glycyrrhizic acid monoglucuronide (GAMG) on acute lung injury induced by single-walled carbon nanotubes (SWCNT) in mice.
      Methods  A total of 30 female C57/BL mice, aged 7-8 weeks, were randomly divided into 3 groups, namely the negative control group (normal saline 40 μg/trachea), the SWCNT model group (SWCNT 40 μg/trachea), and the GAMG treatment group (SWCNT 40 μg/trachea + GAMG 200 mg/kg). The mice in the GAMG treatment group were given GAMG intraperitoneally once a day for 3 days, while the mice in the other groups were given blank solvent at the same time. The pathological changes of lung tissue and the changes of interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) in bronchoalveolar lavage fluid (BALF) were observed, the protein expression of the TLR4/MyD88/NF-κB signal pathway was detected by immunohistochemistry, and the contents of NF-κB and HSP47 were detected by immunofluorescence.
      Results  The degree of lung injury in the GAMG treatment group was obviously alleviated. Compared with the SWCNT group, the levels of MCP-1 and IL-6 in BALF, the expression of TLR4 and MyD88, and the expression of NF-κB p65 and HSP47 in lung tissue were decreased in the GAMG treatment group (P < 0.01).
      Conclusions  GAMG could significantly ameliorate SWCNT-induced acute lung injury and inhibit the activation of the TLR4/MyD88/NF-κB signal pathway in the lung.

     

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