ArticleFrontiers in pharmacology2025
Therapeutic effects of Jing Si herbal tea for chronic obstructive pulmonary disease: a comprehensive investigation from clinical to basic research.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Jing-Si Herbal Tea as a multitargeted complementary therapy: Evidence from preclinical and clinical studies.Tzu chi medical journalReview
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Chronic obstructive pulmonary disease (COPD), a leading cause of global mortality, significantly impairs health-related quality of life (HRQL). COPD is characterized by airway inflammation and lung tissue damage. Jing Si herbal tea (JSHT) has anti-inflammatory effects but has not been explored for treating COPD. This study investigated the potential of JSHT as an adjuvant therapy for COPD. Methods: This study focused on patients with COPD in the exacerbation and stable phases. The control group received the standard treatment, and the JSHT group received the standard treatment plus JSHT. Both groups underwent HRQL assessments, blood tests, and cellular studies involving five different groups to assess the effect of JSHT on damage-associated molecular patterns (DAMPs) and inflammatory markers. Results: Among patients with exacerbations, the JSHT group showed significant improvements in HRQL, including reductions in cough, phlegm, chest tightness, breathlessness, sleep, and anxiety (all p < 0.05). Among patients with stable COPD, the JSHT group showed significant reductions in cough, phlegm, and breathlessness (all p < 0.05). Cellular studies on lipopolysaccharide (LPS)-stimulated A549 cells demonstrated that JSHT effectively reduced the release of DAMPs such as HMGB1, FPR1, and extracellular ATP, and decreased the expression of inflammatory markers including pMAPK, pJNK, NF-kB, and cCaspase 3, and pro-inflammatory cytokines like IL-1, IL-6, IL-8, and TNF-α post-LPS induction. Conclusion: JSHT improved the HRQL in patients with COPD, both in stable and exacerbated states. Cellular models demonstrated a reduction in DAMPs and inflammation, suggesting the potential of JSHT as a therapeutic agent for COPD through modulation of inflammatory responses.
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