[1]杨媛,朱佳.基于Janus激酶2-信号转导器和转录激活因子3-孤独核受体通路探讨人参皂苷Rg1对慢性阻塞性肺疾病模型肺功能的影响[J].陕西医学杂志,2025,54(10):1331-1336.[doi:DOI:10.3969/j.issn.1000-7377.2025.10.006]
　YANG Yuan,ZHU Jia.Effects of ginsenoside Rg1 on lung function in a chronic obstructive pulmonary disease model via the JAK2-STAT3-RORγt pathway[J].,2025,54(10):1331-1336.[doi:DOI:10.3969/j.issn.1000-7377.2025.10.006]
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基于Janus激酶2-信号转导器和转录激活因子3-孤独核受体通路探讨人参皂苷Rg1对慢性阻塞性肺疾病模型肺功能的影响

《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
54
期数:
2025年10期
页码:
1331-1336
栏目:
基础研究
出版日期:
2025-10-05

文章信息/Info

Title:
Effects of ginsenoside Rg1 on lung function in a chronic obstructive pulmonary disease model via the JAK2-STAT3-RORγt pathway
作者:
杨媛; 朱佳
（新疆维吾尔自治区人民医院综合保健内科三病区，新疆 乌鲁木齐 830001）
Author(s):
YANG Yuan; ZHU Jia
(The Third Ward of Comprehensive Healthcare Internal Medicine Department,Xinjiang Uygur Autonomous Region People’s Hospital,Urumqi 830001，China)
关键词:
慢性阻塞性肺疾病; 人参皂苷Rg1; 炎症; Janus激酶2; 信号转导与转录激活因子3; 孤独
Keywords:
Chronic obstructive pulmonary disease; Ginsenoside rg1; Inflammation; JAK2; STAT3; RORγt
分类号:
R 563.1
DOI:
DOI:10.3969/j.issn.1000-7377.2025.10.006
文献标志码:
A
摘要:
目的：基于JAK2-STAT3-RORγt通路探究人参皂苷Rg1对慢性阻塞性肺疾病（COPD）模型肺功能的影响。方法：将50只4~5周龄的大鼠随机分为对照组、模型组、人参皂苷Rg1低剂量组（5 mg/kg）、人参皂苷Rg1高剂量组（20 mg/kg）和人参皂苷Rg1高剂量+CA1组（20 mg/kg+4 mg/kg），每组10只。通过烟熏法构建COPD大鼠模型。肺功能检测仪检测用力肺活量（FVC）、第0.1秒用力呼气容积（FEV0.1）和呼气峰流速（PEF），血气分析仪检测动脉氧分压（PaO2）、血氧饱和度（SaO2）和动脉二氧化碳分压（PaCO2），酶联免疫吸附（ELISA）检测肺泡灌洗液中炎症因子白细胞介素-6（IL-6）、IL-17、肿瘤坏死因子-α（TNF-α）水平，HE染色观察肺组织形态变化，Western blot法检测肺组织中Janus激酶2（JAK2）、信号转导与转录激活因子3（STAT3）、磷酸化信号转导与转录激活因子3（p-STAT3）和孤独核受体（RORγt）的蛋白表达水平。结果：与对照组比较，模型组中大鼠肺组织损伤程度加重，FVC、FVC0.1、PEF、PaO2和SaO2水平降低（均P<0.05），PaCO2、IL-6、IL-17、TNF-α、JAK2、STAT3、p-STAT3和RORγt的蛋白表达水平升高（均P<0.05）。与模型组比较，人参皂苷Rg1高剂量组大鼠肺组织损伤程度减轻，FVC、FVC0.1、PEF、PaO2和SaO2水平升高（均P<0.05），PaCO2、IL-6、IL-17、TNF-α水平、JAK2、STAT3、p-STAT3和RORγt的蛋白表达水平降低（均P<0.05）。与人参皂苷Rg1低剂量组比较，人参皂苷Rg1高剂量组大鼠肺组织损伤程度减轻，FVC、FVC0.1、PEF、PaO2和SaO2水平升高（均P<0.05），PaCO2、IL-6、IL-17、TNF-α水平、JAK2、STAT3、p-STAT3和RORγt的蛋白表达水平降低（均P<0.05）。与人参皂苷Rg1高剂量组比较，人参皂苷Rg1高剂量+CA1组大鼠肺组织损伤程度加重，FVC、FVC0.1、PEF、PaO2和SaO2水平降低（均P<0.05），PaCO2、IL-6、IL-17、TNF-α水平、JAK2、STAT3、p-STAT3和RORγt的蛋白表达水平升高（均P<0.05）。结论： 人参皂苷Rg1能降低炎症因子水平，改善COPD大鼠肺功能，其机制可能与抑制JAK2-STAT3-RORγt信号通路有关。
Abstract:
Objective:To investigate the effects of ginsenoside Rg1 on lung function in a chronic obstructive pulmonary disease (COPD) model via the JAK2-STAT3-RORγt pathway.Methods:Fifty 4- to 5-week-old rats were randomly divided into 5 groups: control group,model group,low-dose ginsenoside Rg1 group (5 mg/kg),high-dose ginsenoside Rg1 group (20 mg/kg),and high-dose ginsenoside Rg1+CA1 group (20 mg/kg+4 mg/kg),with 10 rats in each group.A rat model of COPD was established by cigarette smoke exposure Lung function was assessed using a pulmonary function tester to measure forced vital capacity (FVC),forced expiratory volume at 0.1 seconds (FEV0.1),and peak expiratory flow (PEF).Arterial blood gas analysis was performed to determine partial pressure of oxygen (PaO2),oxygen saturation (SaO2),and partial pressure of carbon dioxide (PaCO2).Enzyme-linked immunosorbent assay (ELISA) was used to detect levels of inflammatory cytokines IL-6,IL-17 and TNF-α in bronchoalveolar lavage fluid.Lung tissue morphology was observed by HE staining.Western blot was employed to analyze the protein expression levels of JAK2,STAT3,p-STAT3 and RORγt in lung tissues.Results:Compared with the control group,the model group exhibited severe lung tissue damage,decreased FVC,FEV0.1,PEF,PaO2,and SaO2 levels (all P<0.05),and increased PaCO2,IL-6,IL-17,TNF-α levels,and protein expression of JAK2,STAT3,p-STAT3,and RORγt(all P<0.05).In contrast,the high-dose ginsenoside Rg1 groups showed alleviated lung tissue injury,increased FVC,FEV0.1,PEF,PaO2,and SaO2 levels (all P<0.05),and decreased PaCO2,IL-6,IL-17,TNF-α levels,and JAK2,STAT3,p-STAT3,and RORγt protein expression (all P<0.05) compared with the model group.The high-dose ginsenoside Rg1 group demonstrated more pronounced improvements in lung function and greater reductions in inflammatory parameters and pathway activation than the low-dose group(all P<0.05).Compared with the high-dose ginsenoside Rg1 group,the high-dose ginsenoside Rg1+CA1 group showed exacerbated lung tissue damage,reduced lung function indices,increased inflammatory cytokine levels,and upregulated JAK2-STAT3-RORγt pathway activation(all P<0.05).Conclusion:Ginsenoside Rg1 improves lung function in COPD model rats by reducing inflammatory cytokine levels,and its mechanism may be associated with the inhibition of the JAK2-STAT3-RORγt signaling pathway.

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备注/Memo:
新疆维吾尔自治区卫生健康保健科研专项课题（BL202404）
更新日期/Last Update: 2025-10-09