| 摘要: |
| 目的:探讨高良姜素(GA)对支气管哮喘(BA)幼年小鼠气道炎症及核苷酸结合寡聚化结构域样受体蛋白3(NLRP3) / 白
细胞介素-1β(IL-1β)信号通路的影响。方法:构建BA 幼年小鼠模型,将所有实验小鼠分为对照组、BA 组和GA 低、中、高剂量
组(GA-L、GA-M、GA-H 组)及GA 高剂量+NLRP3 激活剂尼日利亚菌素组(GA-H+Nig 组)。检测各组小鼠肺泡灌洗液中炎症细
胞总数、嗜酸粒细胞(EOS)计数、中性粒细胞(NEU)计数、淋巴细胞(LYM)计数;采用酶联免疫吸附试验(ELISA)法检测各组小
鼠肺泡灌洗液中炎症因子转化生长因子-β1(TGF-β1)、白细胞介素-10(IL-10)、IL-17、IL-6 水平;苏木精-伊红(HE) 染色观察各
组小鼠支气管病理形态改变;高碘酸-无色品红(PAS) 染色观察各组小鼠气道上皮杯状细胞变化;Western blot 法检测NLRP3、
IL-1β 蛋白表达情况。结果:与对照组比较,BA 组幼年小鼠肺组织异常,支气管管壁结构破坏,大量炎症细胞浸润,气道杯状细
胞及黏液明显增多,肺组织蓝紫色明显,炎症细胞总数、EOS、NEU、LYM 增多,IL-17、IL-6 水平上升,NLRP3、IL-1β 表达上升,
TGF-β1、IL-10 水平下降(P<0. 05);与BA 组相比,GA-L、GA-M、GA-H 组幼年小鼠肺组织和支气管管壁损伤逐渐减轻,炎症细胞
浸润减少,气道上皮杯状细胞及黏液减少,肺组织蓝紫色减少,炎症细胞总数、EOS、NEU、LYM 减少,IL-17、IL-6 水平下降,
NLRP3、IL-1β 表达下降,TGF-β1、IL-10 水平上升(P<0. 05);与GA-H 组相比,GA-H+Nig 组幼年小鼠肺组织和支气管管壁损伤
加重,气道上皮杯状细胞及黏液增多,肺组织蓝紫色增多,炎症细胞总数、EOS、NEU、LYM 增多,IL-17、IL-6 水平上升,NLRP3、
IL-1β 表达上升,TGF-β1、IL-10 水平下降(P<0. 05)。结论:GA 可以通过抑制NLRP3/ IL-1β 信号通路减轻哮喘幼年小鼠的气道
炎症反应。 |
| 关键词: 高良姜素 核苷酸结合寡聚化结构域样受体蛋白3/ 白细胞介素-1β 信号通路 哮喘 气道炎症 |
| DOI：doi:10.13407/j.cnki. jpp.1672-108X.2024.11.001 |
|
| 基金项目:基金项目:2022 年武威市科技局科技计划项目,武威市自然科学基金项目,编号WW2202RPZ038。 |
|
| Effects of Galangin on Airway Inflammation in Juvenile Mice with Asthma by Regulating Nucleotide-Binding Oligomerized Domain-Like Receptor Protein 3 / Interleukin-1β Signaling Pathway |
| Zhang Jincun, Li Yuling |
| (Wuwei Liangzhou Hospital, Gansu Wuwei 733000, China) |
| Abstract: |
| Objective: To probe into the effects of galangin (GA) on airway inflammation in juvenile mice with bronchial asthma (BA)
by regulating nucleotide-binding oligomerized domain-like receptor protein 3 (NLRP3) / interleukin-1β (IL-1β) signaling pathway.
Methods: The juvenile BA mice model was established and all mice were divided into the control group, BA group, low-, medium- and
high-dose GA groups (GA-L, GA-M and GA-H groups) and high-dose GA +NLRP3 activator Nigeriectin group (GA-H+Nig group).
The total number of inflammatory cells, eosinophils (EOS), neutrophils (NEU), and lymphocytes (LYM) in the alveolar lavage fluid
of mice in each group were detected. The levels of inflammatory factors transforming growth factor-β1 (TGF-β1), interleukin-10
(IL-10), IL-17 and IL-6 in alveolar lavage fluid of mice in each group were detected by enzyme linked immunosorbent assay (ELISA).
Hematoxylin-Eeosin staining was applied to observe the pathological changes in the bronchial morphology of mice in each group. Periodic
Acid-Schiff (PAS) staining was applied to observe the changes of goblet cells in the airway epithelium of mice in each group. The
expression of NLRP3 and IL-1β proteins was detected by Western blot. Results: Compared with the control group, the lung tissue of
juvenile mice in the BA group showed abnormalities, structural destruction of the bronchial tube wall, infiltration of a large number of
inflammatory cells, a great increase in airway goblet cells and mucus, and lung tissue was bluish and purple, total number of
inflammatory cells, EOS, NEU and LYM increased, the levels of IL-17 and IL-6 increased, and the expressions of NLRP3 and IL-1β
increased, while the levels of TGF-β1 and IL-10 decreased (P<0. 05). Compared with the BA group, the damage to lung tissue and
bronchial wall of juvenile mice in the GA-L, GA-M, and GA-H groups decreased, infiltration of inflammatory cells decreased, airway
goblet cells and mucus decreased, and lung tissue bluish-purple decreased, total number of inflammatory cells, EOS, NEU and LYM
decreased, the levels of IL-17 and IL-6 decreased, and the expressions of NLRP3 and IL-1β decreased, while the levels of TGF-β1 and
IL-10 increased (P<0. 05). Compared with the GA-H group, the damage to lung tissue and bronchial wall of juvenile mice in the GAH+
Nig group worsened, with an increase in airway goblet cells and mucus, the lung tissue bluish-purple increased, total number of
inflammatory cells, EOS, NEU and LYM increased, the levels of IL-17 and IL-6 increased, and the expressions of NLRP3 and IL-1β increased, while the levels of TGF-β1 and IL-1 decreased (P<0. 05). Conclusion: GA can alleviate airway inflammation in juvenile
mice with BA by inhibiting the NLRP3/ IL-1β signaling pathway. |
| Key words: galangin nucleotide-binding oligomerization domain-like receptor protein 3/ interleukin-1β signaling pathway asthma airway inflammation |
