Sulforaphane attenuates acute lung injury by inhibiting oxidative stress via Nrf2/HO-1 pathway in a rat sepsis model.

Sulforaphane (SFN), an antioxidant derived from cruciferous vegetables, exerts antioxidant capacity and protects organ against oxidative damage. However, the effects of SFN on sepsis-induced acute lung injury (ALI) have not been determined. The aim of this study was to investigate the effect of SFN in sepsis-induced ALI and the role of Nrf2/HO-1 in this process. Rats were subjected to either sham-operated or cecal ligation and puncture-induced sepsis without or with SFN. Pulmonary oxidative stress was significantly increased (reduced SOD activity, enhanced 8-OHdG concentration, elevated 15-F2t-isoprostane level, and enhanced 4-HNE expression) in sepsis that were associated with elevated lung injuries (Increased lung injury index, elevated lung water content, and reduced endothelial barrier integrity). Supplementation of SFN significantly enhanced Nrf2 and HO-1 protein expression in the lungs in sepsis. Further, SFN dose-dependently reduced pulmonary oxidative stress and attenuated lung injuries in sepsis. However, these beneficial effects of SFN were reduced by HO-1 inhibition. Therefore, we concluded that SFN attenuated ALI in sepsis by reducing oxidative stress through activating Nrf2/HO-1. IJCEP