Wang Xinheng, Shao Xiaohan, Li Tongtong, Zhang Lu, Yang Qinjun, Ye Weidong, Tong Jiabing, Li Zegeng, Fang Xiangming
College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei 230038, China.
Anhui Province Key Laboratory of the Application and Transformation of Traditional Chinese Medicine in Prevention and Treatment of Major Pulmonary Diseases, Hefei 230031, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2025 Jun 20;45(6):1153-1162. doi: 10.12122/j.issn.1673-4254.2025.06.05.
To explore the mechanism of Formula (PCN) for inhibiting airway inflammation in rats with asthmatic cold syndrome.
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 (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.
The rat models had obvious manifestations of asthmatic cold syndrome with significantly decreased body mass, food intake, and water intake, reduced FEV, FVC, and FEV/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.
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.
探讨平喘方（PCN）抑制哮喘寒证大鼠气道炎症的机制。
将105只SD大鼠随机均分为7组，包括对照组、哮喘寒证模型组、PCN高、中、低剂量3个治疗组、桂龙咳喘宁（GLCKN）治疗组和地塞米松（DEX）治疗组。除对照大鼠外，其余大鼠均建立哮喘寒证模型，造模开始29天后每日灌胃给予生理盐水、PCN、GLCKN或DEX。观察大鼠的一般状况、肺功能及肺组织病理学变化，分析肺泡灌洗液（BALF）中的炎症因子、氧化应激、肺组织超微结构、细胞因子水平以及与HMGB1/Beclin-1轴和自噬相关基因的表达。
大鼠模型具有明显的哮喘寒证表现，体重、食量和饮水量显著下降，FEV、FVC及FEV/FVC降低，肺组织有明显的炎症细胞浸润，肺泡炎症评分及BALF中中性粒细胞、嗜酸性粒细胞、淋巴细胞、巨噬细胞和白细胞计数增加。大鼠模型的MDA水平显著升高，SOD水平降低，肺组织呈现明显的超微结构改变，HMGB1、Beclin-1、ATG5、TNF-α、IL-6、IL-1β、IL-13的表达及LC3II/I比值升高，而Bcl-2和IFN-γ水平降低。PCN治疗显著改善了大鼠模型的这些病理变化，其治疗效果优于桂龙咳喘宁，与地塞米松相似。
PCN可能通过调节HMGB1/Beclin-1信号轴抑制细胞自噬，从而减轻气道炎症损伤，有效缓解哮喘寒证大鼠模型的气道炎症。
