Lianhua Qingke granules alleviate cigarette smoke-induced COPD through AMPK signaling pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disorder characterized by inflammation, oxidative stress, and airflow limitation, commonly associated with cigarette smoke exposure and aging. Lianhua Qingke Granules (LHQK), derived from Maxing Shigan Decoction and Qingjin Huatan Decoction, is a traditional Chinese medicine historically used to "disperse lung Qi, clear heat, resolve phlegm, and relieve cough." LHQK has shown promise in alleviating respiratory disorders, including reducing inflammation and improving pulmonary function in COPD. However, its underlying mechanisms remain insufficiently explored.

AIM OF THE STUDY: This study aims to investigate the therapeutic effects and mechanisms of LHQK in cigarette smoke-induced COPD models.

MATERIALS AND

METHODS

C57BL/6J mice were exposed to cigarette smoke for three months and treated with high- or low-dose LHQK for three months. Lung tissues were analyzed using histology, transcriptomics, RT-PCR, and western blotting to evaluate inflammation, cellular senescence, and pathway activation. Key cytokines (IL-6, CXCL15, TNF-α) and markers of senescence (p16, p21, p53) were measured.

RESULTS

Our results demonstrated that both low- and high-dose LHQK significantly alleviated lung injury and inflammation in the COPD mouse model, with the high-dose group exhibiting more pronounced effects. Histological analysis and reduced levels of inflammatory cytokines (IL-6, CXCL15, TNF-α) in the LHQK-treated groups compared to the control and COPD groups confirmed the efficacy of LHQK in mitigating lung damage. RNA sequencing of lung tissue from the control, COPD, and LHQK-treated groups revealed that LHQK, particularly at the high dose, regulated the AMPK signaling pathway, which is implicated in aging-related processes. Furthermore, both dose groups of LHQK reduced cellular senescence and alleviated age-related exacerbations of COPD, with the high-dose treatment demonstrating stronger effects. These findings suggest that LHQK protects against smoke-induced COPD by modulating inflammation and cellular senescence through the AMPK signaling pathway.

CONCLUSION

LHQK provides protective effects against smoke-induced COPD by attenuating inflammation and cellular senescence through the AMPK pathway. These findings highlight its potential as an adjunctive therapy for COPD, particularly in aging populations.