A traditional formula protected lungs in sepsis by restoring macrophage mitophagy — in mice and cells
Edited by Samael A. Tejada, Founder & Editor-in-Chief
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The Yiqi Huoxue Jiedu Formula (YHJF) protected against sepsis-associated lung injury in a mouse sepsis model and in cultured macrophages by restoring PINK1/Parkin mitophagy, limiting mitochondrial DNA release and STING inflammation (Chinese Medicine, November 9, 2026). The evidence is preclinical — female mice only, with a cross-species serum method in vitro — and no patient trial is reported.
In sepsis, the lung's own immune cells can become the source of the damage when their damaged mitochondria spill DNA into the cell. This formula appears to restart the cleanup crew — in mice.
What did YHJF do in the macrophages?
In LPS-stimulated MH-S alveolar macrophages, YHJF restored mitochondrial homeostasis by activating PINK1/Parkin-dependent mitophagy — the selective recycling system that removes damaged mitochondria before they leak their contents. With mitophagy restored, less mitochondrial DNA escaped, and the mtDNA-STING signaling axis that converts that leak into inflammatory output was modulated downward. It is a coherent mechanism chain: damaged mitochondria → leaked mtDNA → STING inflammation → lung injury, interrupted at the first step.
What happened in the septic mice?
The in vivo arm used cecal ligation and puncture, the standard polymicrobial sepsis model, in female BALB/c mice randomized to sham surgery, CLP alone, CLP plus low, medium or high YHJF doses, or dexamethasone as a positive control. Per the report, YHJF alleviated lung damage and systemic inflammation in the septic mice, consistent with the macrophage mechanism seen in vitro. Sepsis mouse models are notoriously imperfect predictors of human sepsis — a field littered with mouse successes that failed in ICUs — which is why the mechanism, not the outcome alone, is the contribution here.
What are the stated limits?
The study names two. First, only female mice were used, leaving possible sex-dependent differences in sepsis responses untested. Second, the cell experiments used rat-derived YHJF-containing serum in mouse-derived cell lines — a strategy widely used in traditional Chinese medicine research, but one that introduces interspecies variability. Add the standing cautions for any multi-herb formula: composition standardization and human pharmacology remain open questions, and no sepsis patient should read a mouse CLP study as a treatment signal.
Frequently asked questions
What is YHJF?
Yiqi Huoxue Jiedu Formula, a traditional Chinese medicine formula used clinically for nearly two decades, here tested for sepsis-associated lung injury in mice and macrophages.
How did it protect the lungs?
By activating PINK1/Parkin-dependent mitophagy in alveolar macrophages, restoring mitochondrial homeostasis, limiting mitochondrial DNA release and the STING inflammation it triggers (Chinese Medicine, 2026).
Is this a sepsis treatment?
No. It is a preclinical finding in female mice and a cell line, with limits the authors state themselves. Human sepsis trials would be needed before any clinical claim.
Where the evidence stands
- Established: Mitochondrial DNA release activating STING inflammation is an established injury pathway; PINK1/Parkin mitophagy is the core mitochondrial quality-control system; CLP is the standard mouse sepsis model, with known translational limits.
- Preliminary: YHJF's lung protection: one study (Chinese Medicine, 2026) in one mouse sepsis model (females only) plus one macrophage cell line, with a rat-serum in vitro method the authors flag for interspecies caution.
- Absent: Human evidence — no clinical trial of YHJF for sepsis-associated lung injury is reported, and no dosing or safety data in sepsis patients.
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