Shikonin ameliorates lipoteichoic acid‑induced acute lung injury via promotion of neutrophil apoptosis.

Abstract

Shikonin is the major active component in Lithospermumerythrorhizon and has pharmacological effects including reducing inflammation, aiding resistance to bacteria and promoting wound healing. However, the effect of shikonin on lipoteichoic acid(LTA)‑induced acute lung injury(ALI) remains to be elucidated. ALI is a serious illness resulting from significant pulmonary inflammation caused by various diseases, such as sepsis, acid aspiration and trauma. The present study found that shikonin significantly attenuated LTA‑induced ALI. Following shikonin treatment, the accumulation of pulmonary neutrophils and expression of TNFα, IL‑1β and IL‑6 were decreased in mice with LTA‑induced ALI. Furthermore, Shikonin promoted neutrophil apoptosis by increasing the activation of caspase‑3 and reducing the expression of the antiapoptotic myeloid cell leukemia‑1(Mcl‑1) protein. However, shikonin treatment did not influence the expression of B‑cell lymphoma‑2. The findings of the present study demonstrated that shikonin protected against LTA‑induced ALI by promoting caspase-3 and Mcl‑1‑related neutrophil apoptosis, suggesting that shikonin is a potential agent that can be used in the treatment of sepsis‑mediated lung injury.