Effective-Component Compatibility of Bufei Yishen Formula III Improves Chronic Obstructive Pulmonary Disease by Inhibiting Inflammatory Responses Through Blocking PTX3 Activation.

BACKGROUND AND AIM: For chronic obstructive pulmonary disease (COPD), Bufei Yishen formula (BYF) is an established therapy for COPD, and its effective component compatibility of BYF III (ECC-BYF III) demonstrates comparable efficacy. However, the underlying mechanisms of ECC-BYF III in COPD treatment remain unclear. We aimed to identify the pivotal genes in COPD and explore the mechanism by which ECC-BYF III exerts its effects. EXPERIMENTAL PROCEDURE: A rat model of COPD was established to evaluate the effects of ECC-BYF III treatment. Transcriptomics was used to identify the genes associated with COPD. Based on the transcriptomics and COPD patient gene expression profiles, key genes were screened and verified both in vitro and in vivo. By overexpressing or knocking out pentraxin-related protein 3 (PTX3), the levels of NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) and phospho-Stress-Activated protein kinase/Jun N-terminal kinase (p-SAPK/JNK) were detected to validate the role of ECC-BYF III in regulating PTX3 to suppress inflammation. RESULTS AND CONCLUSION: ECC-BYF III improved lung function and inflammation in COPD rats. Based on transcriptomics, 192 expression genes between the normal and COPD groups were identified. Of these, eight genes were reversed after ECC-BYF III treatment as key genes. Next, the expression levels of key genes were validated in vitro and in vivo, and ECC-BYF III was found to decrease the levels of PTX3. After transfection with the PTX3 plasmid, PTX3 levels significantly increased, whereas the inhibitory effects of ECC-BYF III on NLRP3, p-SAPK/JNK, and inflammation were blocked. In conclusion, PTX3 is a key target of ECC-BYF III in COPD patients. ECC-BYF III regulates PTX3 to inhibit the inflammatory response mediated by NLRP3 and p-SAPK/JNK to improve COPD.