6β-Acetoxysandaracopimaradien-1α,9α-diol (ASPD) reduced cytokines and signaling phosphorylation in LPS-stimulated lung cells and reduced histologic injury, edema, and inflammatory infiltration in an acute-lung-injury mouse model. This supports preclinical Src, MAPK, and Akt/GSK-3β associations, not a human ARDS treatment.
Key findings
- ASPD reduced inflammatory cytokines and phosphorylation of JNK1/2, ERK1/2, p38 MAPK, Akt, and GSK-3β in cells. In mice it reduced histology injury, edema, infiltration, IL-6, TNF-α, and MPO without apparent toxicity, while lowering lung Src/ERK1/2 staining and showing predicted target docking.
Why this matters globally
The work identifies a lead compound and pathways for medicinal chemistry and pharmacology, but LPS models only part of human ARDS.
Thai researcher contribution
The Thai collaboration spans natural-product isolation, chemistry, computation, cell biology, and animal experimentation across three universities.
Limitations to consider
Sample size, dose-response, comparator, and pharmacokinetics are absent from the abstract. Docking does not prove direct binding; pathway changes may follow reduced inflammation, without target knockout/rescue. Acute LPS does not capture infection, ventilation, or ARDS heterogeneity, and human safety is unknown.
Verify the original sources
International Journal of Molecular SciencesRead the original article↗DOI: 10.3390/ijms27135969