ArticleJournal of inflammation research2026
Effective-Component Compatibility of Bufei Yishen Formula III Improves Chronic Obstructive Pulmonary Disease by Inhibiting Inflammatory Responses Through Blocking PTX3 Activation.
Article in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.