Shengmai Powder regulates alveolar macrophage PPAR-γ and improves the chronic inflammatory state of chronic obstructive pulmonary disease

• Dongmei Liu ^[1] ; Zongwei Liu ^[1] ; Xunxun Ma ^[1] ; Shengjie Wang ^[2] ; Jie Lin ^[1] ; Xiuyan Shi ^[1] ; Xiaoyong Xu ^[3]
  1. [1] Nanjing University of Chinese Medicine

     Nanjing University of Chinese Medicine

     China

     
  2. [2] Nanjing Medical University

     Nanjing Medical University

     China

     
  3. [3] Department of Pulmonary and Critical Care Medicine, The Fourth Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China

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• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 52, Nº. 5, 2024, págs. 73-79
• Idioma: inglés
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  • This study examines the therapeutic effects of Shengmai Powder (SMP) on both in vitro and in vivo models of chronic obstructive pulmonary disease (COPD) and the underlying mechanisms. Cigarette smoke and cigarette extracts were used to create in vitro and in vivo models of COPD. ELISA was used to measure the levels of pro-inflammatory factors (IL-6, TNF-α, and IL-1β) in mouse lung tissue and alveolar macrophages. Flow cytometry assessed the phagocytic capacity of alveolar macrophage. Western blotting was used to analyze the expression of RhoA, PPARγ, IκBα, p-IκBα, P65, and p-P65 in alveolar. The results show that SMP reversed the increased levels of pro-inflammatory factors (IL-6, TNF-α, and IL-1β) in mouse lung tissue and alveolar macrophages induced by cigarette smoke and cigarette extract. SMP also restored the decreased fluorescence intensity and RhoA levels in alveolar macrophages caused by cigarette extract. Additionally, SMP increased PPARγ expression and decreased IκBα and P65 phosphorylation in alveolar macrophages exposed to cigarette extract. Also, the effects of SMP were reversed by PPARγ inhibitors. The study concluded that SMP regulates alveolar macrophage phagocytic function through the PPAR-γ/NF-κB pathway, thereby improving the chronic inflammatory state of COPD.