Triptonide curbs macrophage glycolysis to ease sepsis-related lung injury

  • Triptonide, a diterpenoid from Tripterygium wilfordii, was tested in mouse endotoxemia and caecal ligation and puncture models of sepsis-associated lung injury.
  • It limited macrophage pro-inflammatory activation, reduced lung inflammation, oedema and apoptosis, and improved survival.
  • Transcriptomic and metabolic analyses showed suppressed aerobic glycolysis in inflammatory macrophages, via the STAT3/HIF-1α axis.
💡 Points Based on the abstract

Triptonide is a notoriously narrow-window Tripterygium compound, so I'd want the therapeutic index before any mechanism claim. Dosing after CLP onset, not just pre-treatment, plus a STAT3 or HIF-1α rescue to prove the axis is causal, would tell me far more. Glycolysis suppression in macrophages also risks blunting host defence against the infection itself.

Triptonide alleviates sepsis‐associated acute lung injury by suppressing the STAT3/HIF‐1α‐mediated aerobic glycolysis in macrophages ↗