平喘宁方通过调控HMGB1/Beclin-1轴介导的自噬改善患寒哮证大鼠的气道炎症

doi:10.12122/j.issn.1673-4254.2025.06.05

南方医科大学学报 ›› 2025, Vol. 45 ›› Issue (6): 1153-1162.doi: 10.12122/j.issn.1673-4254.2025.06.05

平喘宁方通过调控HMGB1/Beclin-1轴介导的自噬改善患寒哮证大鼠的气道炎症

王心恒¹^,²(), 邵小涵³, 李童童³, 张璐¹, 杨勤军¹^,²^,⁵, 叶卫东¹, 童佳兵¹^,²^,⁴^,⁵, 李泽庚¹^,²^,⁴^,⁵, 方向明¹()

^1.安徽中医药大学中医学院，安徽合肥 230038
^2.中医药防治肺系重大疾病应用转化安徽省重点实验室，安徽合肥 230031
^3.安徽中医药大学针推学院，安徽合肥 230038
^4.安徽中医药大学第一附属医院，安徽合肥 230031
^5.安徽省中医药科学院肺病研究所，安徽合肥 230039

收稿日期:2024-12-25 出版日期:2025-06-20 发布日期:2025-06-27
通讯作者: 方向明 E-mail:wangxinheng@ahtcm.edu.cn;fxm.bsh@163.com
作者简介:王心恒，讲师，博士，E-mail: wangxinheng@ahtcm.edu.cn
基金资助:
国家自然科学基金(82074401);安徽省自然科学基金(2108085QH369);安徽中医药大学高层次人才支持计划项目(2020rcyb002);安徽省重点实验室开放课题(2024ZYFBAHKLA10)

Pingchuanning Formula suppresses airway inflammation in a rat model of asthmatic cold syndrome by regulating the HMGB1/Beclin-1 axis-mediated autophagy

Xinheng WANG¹^,²(), Xiaohan SHAO³, Tongtong LI³, Lu ZHANG¹, Qinjun YANG¹^,²^,⁵, Weidong YE¹, Jiabing TONG¹^,²^,⁴^,⁵, Zegeng LI¹^,²^,⁴^,⁵, Xiangming FANG¹()

^1.College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei 230038, China
^2.Anhui Province Key Laboratory of the Application and Transformation of Traditional Chinese Medicine in Prevention and Treatment of Major Pulmonary Diseases, Hefei 230031, China
^3.College of Acupuncture-Moxibustion and Tuina, Anhui University of Chinese Medicine, Hefei 230038, China
^4.First Affiliated Hospital of Anhui University of Chinese Medicine, Hefei 230031, China
^5.Institute of Lung Disease in Anhui Academy of Traditional Chinese Medicine, Hefei 230039, China

Received:2024-12-25 Online:2025-06-20 Published:2025-06-27
Contact: Xiangming FANG E-mail:wangxinheng@ahtcm.edu.cn;fxm.bsh@163.com
Supported by:
National Natural Science Foundation of China(82074401)

摘要/Abstract

摘要：

目的基于高迁移率族蛋白 B1（HMGB1）/自噬相关基因Beclin-1（Beclin-1）轴探讨平喘宁方（PCN）调控细胞自噬减轻寒哮证大鼠气道炎症的作用。方法 105只SPF级SD大鼠，随机分为对照组（CON）、模型组（MOD）、平喘宁高、中、低剂量组（PCN-H、PCN-M、PCN-L）、桂龙咳喘宁组（GLCKN）和地塞米松组（DEX），15只/组。除CON组外，其余大鼠构建寒哮证模型，并从第29天开始灌胃PCN、DEX及GLCKN。观察各组大鼠体质量、摄食量、摄水量，肺功能、肺组织氧化应激水平、肺泡灌洗液（BALF）炎性因子、肺组织病理、肺组织超微结构，细胞因子水平以及HMGB1/Beclin-1信号轴和细胞自噬相关基因和蛋白的表达。结果与CON组比较，MOD组大鼠表现出呼吸急促、喘息、流涕、腹部收缩明显、反应迟钝、反应缓慢，进食量减少，明显的皮毛枯槁或脱落等表现；体质量、摄食量、摄水量明显下降（P<0.05）；第0.3秒用力呼气量（FEV_0.3）、用力肺活量（FVC）、FEV_0.3/FVC明显降低（P<0.05）；肺组织表现出明显的炎性浸润，肺泡炎症评分明显上升（P<0.05）；BALF中性粒细胞、嗜酸性粒细胞、淋巴细胞、巨噬细胞、白细胞数量明显上升（P<0.05）；肺组织MDA明显上升，SOD明显下降（P<0.05）；透射电镜（TEM）观察发现MOD组有自噬小泡数量较多，线粒体排列有紊乱及水肿现象，嗜锇性板层小体排空比较明显；肺组织HMGB1、Beclin-1、ATG5蛋白及mRNA表达明显上升，Bcl-2蛋白表达及mRNA明显降低，LC3II/I比值明显上升（P<0.05）；大鼠肺组织细胞因子IFN-γ明显降低，TNF-α、IL-6IL-1β、IL-13明显上升（P<0.05）。与MOD组比较，PCN能明显改善各项指标的病理改变，且作用效果优于GLKCN组，不亚于DEX组（P<0.05）。结论 PCN能有效改善寒哮证模型大鼠气道炎症，其机制可能与调控HMGB1/Beclin-1信号轴，抑制细胞自噬从而缓解炎症损伤有关。

关键词: 支气管哮喘, 平喘宁方, 细胞自噬, 肺功能, 气道炎症, 寒哮证

Abstract:

Objective To explore the mechanism of Pingchuanning Formula (PCN) for inhibiting airway inflammation in rats with asthmatic cold syndrome. Methods A total of 105 SD rats were randomized equally into 7 groups, including a control group, an asthmatic cold syndrome model group, 3 PCN treatment groups at high, medium and low doses, a Guilong Kechuanning (GLCKN) treatment group, and a dexamethasone (DEX) treatment group. In all but the control rats, asthma cold syndrome models were established and daily gavage of saline, PCN, GLCKN or DEX was administered 29 days after the start of modeling. The changes in general condition, lung function and lung histopathology of the rats were observed, and inflammatory factors in the alveolar lavage fluid (BALF), oxidative stress, lung tissue ultrastructure, cytokine levels, and expressions of the genes related to the HMGB1/Beclin-1 axis and autophagy were analyzed. Results The rat models had obvious manifestations of asthmatic cold syndrome with significantly decreased body mass, food intake, and water intake, reduced FEV_0.3, FVC, and FEV_0.3/FVC, obvious inflammatory cell infiltration in the lung tissue, and increased alveolar inflammation score and counts of neutrophils, eosinophils, lymphocytes, macrophages, and leukocytes in the BALF. The rat models also had significantly increased MDA level and decreased SOD level and exhibited obvious ultrastructural changes in the lung tissues, where the expressions of HMGB1, Beclin-1, ATG5, TNF-α, IL-6,IL-1β, and IL-13 and the LC3II/I ratio were increased, while the levels of Bcl-2 and IFN-γ were decreased. PCN treatment significantly improved these pathological changes in the rat models, and its therapeutic effect was better than that of GLKCN and similar to that of DEX. Conclusion PCN can effectively alleviate airway inflammation in rat models of asthmatic cold syndrome possibly by modulating the HMGB1/Beclin-1 signaling axis to suppress cell autophagy, thereby attenuating airway inflammatory damages.

Key words: bronchial asthma, Pingchuanning Formula, cell autophagy, lung function, airway inflammation, asthmatic cold syndrome

王心恒, 邵小涵, 李童童, 张璐, 杨勤军, 叶卫东, 童佳兵, 李泽庚, 方向明. 平喘宁方通过调控HMGB1/Beclin-1轴介导的自噬改善患寒哮证大鼠的气道炎症[J]. 南方医科大学学报, 2025, 45(6): 1153-1162.

Xinheng WANG, Xiaohan SHAO, Tongtong LI, Lu ZHANG, Qinjun YANG, Weidong YE, Jiabing TONG, Zegeng LI, Xiangming FANG. Pingchuanning Formula suppresses airway inflammation in a rat model of asthmatic cold syndrome by regulating the HMGB1/Beclin-1 axis-mediated autophagy[J]. Journal of Southern Medical University, 2025, 45(6): 1153-1162.

图/表 11

表1 PCN方的中药组成

Tab.1 Composition of Pingchuanning Formula (PCN)

Scientific name	Family	Drug name
Ephedra sinica stapf	Ephedraceae	Chinese ephedra
Prunus armeniaca L.	Rosaceae	Apricot
Citrus reticulata blanco	Rutaceae	Satsuma orenge
Bulbus fritillariae thunbergii	Liliaceae	Bulb of thunberg fritillary
Asarum heterotropoides Fr. Schmidt var.	Aristolochiaceae	Manchur wildginger
Perilla frutescens (L.) Britt.	Lamiaceae	Common perilla
Astragali radix	Fabaceae	Milkvetch root
Radix pseudoxtellariae	Caryophyllaceae	Heterophylly falsestarwort root
Pheretima	Megascolecidae	Earthworm
Pinelliae rhizoma	Araceae	Pinellia ternata
Saposhnikoviae radix	Umbelliferae	Divaricate saposhniovia root

图1 平喘宁寒哮证大鼠模型建立与给药示意图

Fig.1 Schematic diagram of the establishment of the rat model and drug administration.

表2 各检测指标引物

Tab.2 Primers for amplification of the target mRNAs

Gene	Amplicon size (bp)	Forward primer (5'→3')	Reverse primer (5'→3')
GAPDH	127	CAAGGCTGAGAATGGGAAGC	GAAGACGCCAGTAGACTCCA
Beclin-1	134	GAATGAGGGCGACAGTGAAC	CCTGGACCTTCTCCAGGTTT
ATG5	71	TCCTGCCACAGTAAGGGAAG	TCACAGTCAATGGCAGGAGT
HMGB1	85	CCTAAGAAGCCGAGAGGCAA	CATCCGGGTGCTTCTTCTTG-3'
Bcl-2	84	GCCTTCTTTGAGTTCGGTG	GCCAGGAGAAATCAAACAGAG

图2 各组大鼠大鼠体质量、摄食量和摄水量比较

Fig.2 Comparison of body mass (A), food intake (B), and water intake (C) of the rats among the groups. *P<0.05 vs control group, #P<0.05 vs model group.

图3 各组大鼠肺功能指标比较

Fig.3 Comparison of lung function of the rats among the groups. A: FEV0.3; B: FVC; C: FEV0.3/FVC; *P<0.05 vs control group, #P<0.05 vs model group.

图4 各组大鼠肺组织病理学形态和炎症评分比较

Fig.4 Lung histopathology and inflammation scores of the rats in each group (HE staining, scale bar=40 μm). *P<0.05 vs control group, #P<0.05 vs model group (n=6).

图5 各组大鼠氧化应激和炎症因子指标比较

Fig.5 Comparison of inflammatory cell counts in the BALF and oxidative stress factors among the groups. A: Total white cell counts. B: Neu cell counts. C: Eos cell counts. D: Lym cell counts. E: Mac cell counts. F: MDA level. G: SOD level. *P<0.05 vs control group, #P<0.05 vs model group

图6 TEM观察各组大鼠肺组织超微结构

Fig.6 Ultrastructure of lung tissue of rats in each group observed by TEM (Original magnification:×10 000, ×25 000). AP: Autophagosome; AL: Autophagolysosome.

图7 各组大鼠自噬相关mRNA的表达

Fig.7 Expression of autophagy-related mRNAs in the lung tissue of the rats in each group. A: HMGB1 mRNA expression; B: Beclin-1 mRNA expression; C: Bcl-2 mRNA expression; D: ATG5 mRNA expression. *P<0.05 vs control group; #P<0.05 vs model group.

图8 各组大鼠自噬相关蛋白的表达

Fig.8 Expression levels of autophagy-associated proteins in the lung tissue of the rats in the groups. A: HMGB1 expression; B: Western blotting for analyzing HMGB1, Beclin-1, Bcl-2, LC3II/LC3I, and ATG5 expressions in the lung tissue; C: Beclin-1 expression; D: Bcl-2 expression; E: LC3II/LC3I ratio; F: ATG5 expression. *P<0.05 vs control group; #P<0.05 vs model group.

图9 各组大鼠肺组织炎症因子比较

Fig.9 Comparison of lung tissue inflammatory factors among the group. A: IFN-γ expression; B: TNF-α expression; C: IL-1β expression; D: IL-6 expression; E: IL-13 expression. *P<0.05 vs control group; #P<0.05 vs model group (n=8)

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平喘宁方通过调控HMGB1/Beclin-1轴介导的自噬改善患寒哮证大鼠的气道炎症

Pingchuanning Formula suppresses airway inflammation in a rat model of asthmatic cold syndrome by regulating the HMGB1/Beclin-1 axis-mediated autophagy

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