This study explores the therapeutic effect of Shengmai Powder (SMP) on in vitro and in vivo models of chronic obstructive pulmonary disease (COPD) and its underlying mechanisms. COPD in vitro and in vivo models were established using cigarette smoke and cigarette extracts. Elisa detects the levels of promoting factors (IL-6, TNF-α, and IL-1β) in mouse lung tissue and alveolar macrophages. Flow cytometry detects fluorescence intensity representing the phagocytic capacity of alveolar macrophages. Western blot detects the expression of RhoA, PPARγ, IκBα, p-IκBα, P65, and p-P65 in alveolar macrophages. SMP can reverse the increased levels of pro-inflammatory factors (IL-6, TNF-α, and IL-1β) in mouse lung tissue caused by cigarette smoke. SMP can reverse the increased levels of pro-inflammatory factors (IL-6, TNF-α, and IL-1β) in alveolar macrophages caused by cigarette extract. SMP can reverse the decrease in fluorescence intensity and RhoA in alveolar macrophages caused by cigarette extract. SMP can reverse the decrease in fluorescence intensity and RhoA in alveolar macrophages caused by cigarette extract. SMP can reverse the decrease in PPARγ expression and increase in IκBα and P65 phosphorylation in alveolar macrophages caused by cigarette extract. PPARγ inhibitors can reverse the effects of SMP. SMP can regulate the phagocytic function of alveolar macrophages through PPAR-γ/NF-κB pathway and improve the chronic inflammatory state of chronic obstructive pulmonary disease.