Dioscin prevents LPS‑induced acute lung injury through inhibiting the TLR4/MyD88 signaling pathway via upregulation of HSP70.

Dioscin, as a type of important natural steroidal saponin, has widespread sources, primarily from the fenugreek plant, which is an important raw material in the production of synthetic steroid hormone drugs. Dioscin has anti‑tumor, anti‑inflammatory, antioxidant and other significant pharmacological effects with high medicinal value. The present work aimed to research the protective effect and underlying mechanisms by which dioscin prevents acute lung injury (ALI). Mice were injected with 5 mg/kg LPS to induce lung injury. Mice were treated with dioscin (20, 40 and 60 mg/kg) following LPS‑induced lung injury. Treatment with dioscin significantly decreased total number of alveolar macrophages, water content of lung and total protein concentration in ALI mice. Dioscin treatment significantly suppressed the ALI‑induced interleukin (IL)‑1B, IL‑6, tumor necrosis factor‑α, nuclear factor (NF)‑κB, myeloperoxidase, interferon‑γ and intercellular adhesion molecule‑1 activities in ALI rats. Following this, the authors identified that dioscin significantly also suppressed cyclooxygenase‑2, heat shock protein 70, Toll‑like receptor 4, MyD88 and NF‑κB protein expression in ALI rats. The results suggested that dioscin prevents LPS‑induced ALI through inhibiting the TLR4/MyD88 signaling pathway via upregulation of HSP70.