Celastrol (CEL) was shown to display anti-inflammatory properties, and played an important role in antiapoptosis. There were inflammation mediated by cytokines and apoptosis distinctly in the progression of acute lung injury (ALI) burn-induced. This study was conducted to explore the role of CEL in ALI induced by burns. In order to induce burn injury, rats were exposed to a 92 degrees C water bath for 18 seconds. After burn experiment, the Burn + Celastrol group received CEL, and vehicle (DMSO) was used to treat the rats from Burn + Vehicle group. And the Sham + Burn group received no treatment. Vascular protein leakage was detected by Evans blue (EB) concentration to evaluate the lung microvascular permeability. Then wet-to-dry lung weight ratio (W/D), and hematoxylin and eosin staining (H&E) were measured respectively to investigate interstitial edema, neutrophil recruitment, and histopathological changes in lung tissues burn-induced ALI. To explore the mechanism of action of CEL, we assessed levels of inflammatory cytokines by ELISA assay, TUNEL staining and western blotting. Then we detected apoptosis-related factors, including the amount of apoptotic cells, caspase-3 activity, and Bax or Bcl-xl, respectively. The pulmonary microvascular hyperpermeability, histopathological characteristics, and a high W/D were attenuated by CEL for burn-injury rats. The concentration of cytokines burn-induced ALI from tissues and serum were decreased by CEL. Furthermore, after CEL treatment, TUNEL-positive cells, the protein level of Bax and caspase-3 activity reduced, and the level of Bcl-xl in protein increased. In conclusion, in lung injury burn-induced, CEL has a positive effect on antiinflammation and anti-apoptosis. Thus, CEL could be as a latent for the cure of ALI burn-induced.