Improvement effect and mechanism of desloratadine citrate disodium in hypersensitivity pneumonitis model mice

PENG Wenjuan; ZHAO Yan; YUE Shaoyun; WU Yujiao; MO Jiajia; CHU Zhaoxing

doi:10.6039/j.issn.1001-0408.2025.15.11

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Improvement effect and mechanism of desloratadine citrate disodium in hypersensitivity pneumonitis model mice

更新时间：2025-11-14

- Improvement effect and mechanism of desloratadine citrate disodium in hypersensitivity pneumonitis model mice
- ZHONGGUO YAOFANG Vol. 36, Issue 15, Pages: 1882-1886(2025)
- 作者机构：
  
  1.安徽省胸科医院内三科，合肥　230022
  2.合肥医工医药股份有限公司，合肥　230601
- 作者简介：
- 基金信息：
- DOI：10.6039/j.issn.1001-0408.2025.15.11
  CLC： R965
- Received：28 March 2025，
  
  Revised：2025-04-27，
  
  Accepted：10 July 2025，
  
  Published：15 August 2025
- 稿件说明：
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彭文娟,赵炎,岳少云,等.枸地氯雷他定对小鼠过敏性肺炎的改善作用及机制[J].中国药房,2025,36(15):1882-1886.

PENG Wenjuan,ZHAO Yan,YUE Shaoyun,et al.Improvement effect and mechanism of desloratadine citrate disodium in hypersensitivity pneumonitis model mice[J].ZHONGGUO YAOFANG,2025,36(15):1882-1886.
彭文娟,赵炎,岳少云,等.枸地氯雷他定对小鼠过敏性肺炎的改善作用及机制[J].中国药房,2025,36(15):1882-1886. DOI： 10.6039/j.issn.1001-0408.2025.15.11.

PENG Wenjuan,ZHAO Yan,YUE Shaoyun,et al.Improvement effect and mechanism of desloratadine citrate disodium in hypersensitivity pneumonitis model mice[J].ZHONGGUO YAOFANG,2025,36(15):1882-1886. DOI： 10.6039/j.issn.1001-0408.2025.15.11.

摘要

目的

探讨枸地氯雷他定对小鼠过敏性肺炎（HP）的改善作用及机制。

方法

将60只小鼠按随机数字表法分为空白对照组（生理盐水）、模型组（生理盐水）、泼尼松组（阳性对照，20 mg/kg）和枸地氯雷他定低、中、高剂量组（0.5、1、2 mg/kg），每组10只。除空白对照组外，其余各组小鼠均通过腹腔注射卵清蛋白和吸入卵清蛋白喷雾构建HP模型。从造模第22天开始，各组小鼠灌胃相应药物/生理盐水，每天1次，连续11 d。末次给药后，评估各组小鼠肺功能和气道高反应性，检测血清中白细胞介素（IL）-1β、IL-4、IL-6水平和支气管肺泡灌洗液中IL-8、IL-13、IL-17A水平，观察各组小鼠肺组织Masson染色病理变化，检测肺组织中纤维化相关蛋白转化生长因子β

（TGF-β

）、3型胶

原蛋白（Col-Ⅲ）和纤维连接蛋白（FN）的表达。

结果

与空白对照组比较，模型组小鼠肺功能显著降低（

＜0.01），气道阻力和血清中IL-1β、IL-4、IL-6水平以及支气管肺泡灌洗液中IL-8、IL-13、IL-17A水平均显著升高（

＜0.01）；肺组织出现肺泡塌陷、萎缩及结构紊乱，并生成大量蓝色胶原纤维沉积，阳性染色百分比显著升高（

＜0.01）；肺组织中TGF-β

、Col-Ⅲ和FN蛋白表达水平均显著升高（

＜0.01）。给予枸地氯雷他定干预后，枸地氯雷他定各剂量组小鼠肺组织病理变化均有不同程度改善，以上指标水平大部分显著逆转（

＜0.05或

＜0.01）。

结论

枸地氯雷他定可改善HP小鼠的肺功能和气道高反应性，抑制血清和支气管肺泡灌洗液中炎症因子的释放，降低胶原纤维的沉积，其作用机制可能与抗炎、调节免疫和抗纤维化相关。

Abstract

OBJECTIVE

To investigate the improvement effect and mechanism of desloratadine citrate disodium in mice with hypersensitivity pneumonitis （HP）.

METHODS

Sixty mice were randomly divided into blank control group （normal saline）， model group （normal saline）， prednisone group （positive control， 20 mg/kg） and desloratadine citrate disodium low-， medium- and high-dose groups （0.5， 1， 2 mg/kg）， with 10 mice in each group. Except for the blank control group， mice in other groups were intraperitoneally injected with ovalbumin （OVA） and exposed to OVA inhalation to establish the HP model. On day 22 post-modeling， mice in each group were administered the corresponding drugs or normal saline， once a day， for 11 consecutive days. After the last administration， lung function and airway hyperreactivity were assessed. The levels of interleukin-1β （IL-1β）， IL-4 and IL-6 in serum as well as the levels of IL-8， IL-13 and IL-17A in bronchoalveolar lavage fluid were determined. Pathological changes in lung tissue of mice were evaluated using Masson staining. Furthermore， the expressions of fibrosis-related proteins， including transforming growth factor β

（TGF-β

）， type Ⅲ collagen （Col-Ⅲ） and fibronectin （FN） were determined in lung tissues.

RESULTS

Compared with the blank control group， the model group showed signif

icant deterioration in lung function （

＜0.01）， while airway resistance and serum levels of IL-1β， IL-4， IL-6 and the levels of IL-8， IL-13 and IL-17A in the bronchoalveolar lavage fluid were increased significantly （

＜0.01）. The lung tissues exhibited alveolar collapse， atrophy， and structural disarray， along with the formation of extensive deposits of blue collagen fibers， the percentage of positive staining increased significantly （

＜0.01）. Additionally， the expression levels of TGF-β

， Col-Ⅲ， and FN proteins in the lung tissues were also increased significantly （

＜0.01）. After intervention with desloratadine citrate disodium， the pathological changes in the lung tissues of mice in each dosage group of desloratadine citrate disodium showed varying degrees of improvement， and most of the aforementioned indicator levels were significantly reversed （

＜0.05 or

＜0.01）.

CONCLUSIONS

Desloratadine citrate disodium can improve the lung function and airway hyperreactivity of HP mice， inhibit the release of inflammatory factors in serum and bronchoalveolar lavage fluid， and reduce the deposition of collagen fibers. Its mechanism of action may be related to anti-inflammatory， immunomodulatory， and antifibrotic effects.

关键词

Keywords

references

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