Abstract
COPD is an inflammatory lung disease that limits airflow and remodels the pulmonary vascular system. This study delves into the therapeutic potential and mechanistic underpinnings of Panax notoginseng Saponins (PNS) in alleviating inflammation and pulmonary vascular remodeling in a COPD rat model. Symmap and ETCM databases provided Panax notoginseng-related target genes, and the CTD and DisGeNET databases provided COPD-related genes. Intersection genes were subjected to protein-protein interaction analysis and pathway enrichment to identify downstream pathways. A COPD rat model was established, with groups receiving varying doses of PNS and a Roxithromycin control. The pathological changes in lung tissue and vasculature were examined using histological staining, while molecular alterations were explored through ELISA, RT-PCR, and Western blot. Network pharmacology research suggested PNS may affect the TLR4/NF-κB pathway linked to COPD development. The study revealed that, in contrast to the control group, the COPD model exhibited a significant increase in inflammatory markers and pathway components such as TLR4, NF-κB, HIF-1α, VEGF, ICAM-1, SELE mRNA, and serum TNF-α, IL-8, and IL-1β. Treatment with PNS notably decreased these markers and mitigated inflammation around the bronchi and vessels. Taken together, the study underscores the potential of PNS in reducing lung inflammation and vascular remodeling in COPD rats, primarily via modulation of the TLR4/NF-κB/HIF-1α/VEGF pathway. This research offers valuable insights for developing new therapeutic strategies for managing and preventing COPD.
Acknowledgement
Not applicable.
Ethical approval
All animal experiments strictly followed the NIH “Guide for the Care and Use of Laboratory Animals” and were approved by the Ethics Committee of Yunnan University of Traditional Chinese Medicine.
Authors’ contributions
YNH, NPH and XMZ designed the study. QYF, BQ, OX and BJL collated the data, carried out data analyses and produced the initial draft of the manuscript. YNH, NPH and XMZ contributed to drafting the manuscript. All authors have read and approved the final submitted manuscript.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The data underlying this article will be shared on reasonable request to the corresponding author.