Plain-language summary
Ginsenoside Rb1 was tested in a murine caecal ligation and puncture model of sepsis-associated acute lung injury. Pre-treatment improved survival, reduced pulmonary oedema and tissue injury, and lowered inflammatory cytokine levels in bronchoalveolar lavage fluid. The proposed mechanism centres on the vesicles that alveolar macrophages release: Rb1 suppressed secretion of macrophage-derived extracellular vesicles that damage the alveolar epithelium, and restored the barrier proteins ZO-1, occludin and E-cadherin both in vivo and in vitro. Pathway analysis pointed to NF-kappaB, and validation confirmed that Rb1 reduced NF-kappaB activation in alveolar epithelial cells.
Key findings
- In a caecal ligation and puncture mouse model, ginsenoside Rb1 pre-treatment improved survival and reduced pulmonary oedema and lung injury.
- Inflammatory cytokine levels in bronchoalveolar lavage fluid fell after treatment.
- Rb1 suppressed release of alveolar macrophage-derived vesicles that injure the alveolar epithelium.
- Alveolar barrier proteins ZO-1, occludin and E-cadherin were restored in cell and animal experiments.
- Bioinformatic analysis and follow-up validation implicated reduced NF-kappaB activation in alveolar epithelial cells.
- This is a preclinical murine and cell-culture study; it does not establish that a botanical compound can be used to manage lung injury in patients.
Why this matters for lung repair
The alveolar barrier is what keeps airspaces dry, and its loss is central to acute respiratory failure. What makes this paper relevant beyond the specific compound is the intercellular step it describes: an alveolar macrophage sending vesicles that injure neighbouring epithelial cells. That framing, rather than the botanical itself, is the part that connects to the wider literature JuvGuard tracks on vesicle-mediated communication in the lung. The study is preclinical.
Original abstract
Sepsis-associated acute lung injury (SALI) is a critical complication of sepsis, characterized by alveolar epithelial barrier disruption and excessive inflammation, which contributes substantially to morbidity and mortality. The present study investigates the protective effects of ginsenoside Rb1 on SALI and elucidates its underlying mechanisms involving alveolar macrophage-derived extracellular vesicles (EVs). Using a cecal ligation and puncture (CLP) murine model, LPS-stimulated alveolar macrophages, and EV isolation and characterization, we evaluated Rb1's influence on survival, lung histopathology, inflammatory cytokine levels, alveolar epithelial barrier proteins (ZO-1, Occludin, E-cadherin), and NF-κB signaling. Rb1 pretreatment significantly improved survival, reduced pulmonary edema and tissue injury, and decreased inflammatory cytokines in bronchoalveolar lavage fluid. Mechanistically, Rb1 suppressed the secretion of macrophage-derived EVs that mediate alveolar epithelial injury and restored barrier-associated protein expression both in vitro and in vivo. Bioinformatic analyses identified NF-κB signaling as a key pathway influenced by Rb1-modulated EVs, and experimental validation confirmed that Rb1 attenuated NF-κB activation in alveolar epithelial cells. Collectively, these findings demonstrate that Rb1 alleviates SALI by modulating macrophage-EV-mediated epithelial barrier disruption and inhibiting NF-κB-driven inflammation. This study highlights a novel intercellular mechanism underlying Rb1's protective effects and provides a mechanistic rationale for targeting EV-mediated communication as a therapeutic strategy in sepsis-induced lung injury.
Frequently asked questions
What did this study find?
Ginsenoside Rb1 was tested in a murine caecal ligation and puncture model of sepsis-associated acute lung injury. Pre-treatment improved survival, reduced pulmonary oedema and tissue injury, and lowered inflammatory cytokine levels in bronchoalveolar lavage fluid. The proposed mechanism centres on the vesicles that alveolar macrophages release: Rb1 suppressed secretion of macrophage-derived extracellular vesicles that damage the alveolar epithelium, and restored the barrier proteins ZO-1, occludin and E-cadherin both in vivo and in vitro. Pathway analysis pointed to NF-kappaB, and validation confirmed that Rb1 reduced NF-kappaB activation in alveolar epithelial cells.
Was this tested in humans or in the laboratory?
This is preclinical work — the findings come from laboratory models, not from human participants.
Where can I read the original paper?
The full text lives with the publisher: https://doi.org/10.1016/j.intimp.2026.117394
Does this study prove that JuvGuard works?
No. This is an independent, peer-reviewed study on extracellular vesicles. JuvGuard references the published literature for education only. A single paper cannot establish that any product works, and nothing here is medical advice.
How to cite this paper
Ming Hao, Zhang Yun-Yan, Chen Liu, Yu Yan-Li, Liu Shi-Ping, Zhan Li-Ying et al.. Ginsenoside alleviates sepsis related acute lung injury by inhibiting the destruction of alveolar epithelial barrier mediated by EVs secreted by alveolar macrophages.. International immunopharmacology. 2026, 2026-09-10. DOI: 10.1016/j.intimp.2026.117394
Source & verification
- Journal: International immunopharmacology
- Published: 10 September 2026
- DOI: 10.1016/j.intimp.2026.117394
- PubMed ID: 42721507
- Indexed via: pubmed
- MeSH terms: —