ArticleChinese medicine2026
Yiqi Huoxue Jiedu formula protects against sepsis-associated lung injury by modulating macrophage mitophagy and mtDNA-STING signaling.
Article in Chinese medicine, 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
12 authors.
Funding
Abstract
backgroundYiqi Huoxue Jiedu Formula (YHJF) is a traditional Chinese medicine formula that has been used as an adjunctive therapy for sepsis for nearly two decades. Previous clinical studies showed that YHJF improves Sequential Organ Failure Assessment (SOFA) scores and modulates gut microbiota in elderly patients with pneumonia-associated sepsis. However, the mechanism by which YHJF protects against sepsis-associated acute lung injury (SALI) remains unclear.
methodsA murine SALI model was established by cecal ligation and puncture (CLP). Therapeutic effects were evaluated by histopathology, micro-CT, pulmonary function assessment, and ELISA. Mechanistic studies included proteomic analysis of lung tissues and LPS-stimulated MH-S macrophages, pharmacological modulation with Mdivi-1 and urolithin A (UA), macrophage-epithelial co-culture, HPLC fingerprinting, UPLC-HRMS, and molecular docking.
resultsYHJF significantly improved 7-day survival and ameliorated lung injury, pulmonary edema, respiratory dysfunction, and systemic inflammation in mice with CLP-induced SALI. Proteomic profiling and subsequent functional assays suggested that enhanced mitophagy in macrophages represents a central protective mechanism. In vivo, YHJF increased autophagosome formation and PINK1/Parkin co-localization in BALF-derived alveolar macrophages. In vitro, YHJF restored mitochondrial homeostasis by activating PINK1/Parkin-dependent mitophagy in macrophages. This was accompanied by reduced cytoplasmic mtDNA leakage, downregulated cGAS expression, and suppression of the STING-TBK1-IRF3 pathway and subsequent type I interferon responses. Pharmacological inhibition of mitophagy with Mdivi-1 abolished these protective effects of YHJF, whereas activation with UA augmented them, demonstrating that mitophagy is necessary for YHJF-mediated protection. In a macrophage-epithelial co-culture system, YHJF-treated macrophages alleviated LPS-induced apoptosis in MLE-12 alveolar epithelial cells. Furthermore, chemical analysis integrated with molecular docking identified aloe-emodin, rhein, and genistein as candidate bioactive constituents of YHJF that likely contribute to its regulation of macrophage mitophagy.
conclusionYHJF protects against SALI by restoring macrophage mitophagy and suppressing mtDNA-STING-mediated inflammatory signalling. These findings support YHJF as a potential therapeutic strategy for sepsis-associated lung injury.
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.