Sulforaphane alleviates lung ischemia‑reperfusion injury through activating Nrf‑2/HO‑1 signaling

Abstract

Oxidative stress and inflammation are both involved in the pathogenesis of lung ischemia‑reperfusion (I/R) injury. Sulforaphane (SFN) is a natural product with cytoprotective, anti‑inflammatory, and antioxidant properties. The present study hypothesized that SFN may protect against lung I/R injury via the regulation of antioxidant and anti‑inflammatory‑related pathways. A rat model of lung I/R injury was established, and rats were randomly divided into 3 groups: Sham group, I/R group, and SFN group. It was shown that SFN protected against a pathological inflammatory response via inhibition of neutrophil accumulation and in the reduction of the serum levels of the pro‑inflammatory cytokines, IL‑6, IL‑1β, and TNF‑α. SFN treatment also significantly inhibited lung reactive oxygen species production, decreased the levels of 8‑OH‑dG and malondialdehyde, and reversed the decrease in the antioxidant activities of the enzymes catalase, superoxide dismutase, and glutathione peroxidase in the lungs of the I/R treated rats. In addition, SFN ameliorated I/R‑induced lung apoptosis in rats by suppressing Bax and cleaved caspase‑3 levels and increased Bcl‑2 expression. Furthermore, SFN treatment activated an Nrf2‑related antioxidant pathway, as indicated by the increased nuclear transfer of Nrf2 and the downstream HO‑1 and NADPH quinone oxidoreductase‑1. In conclusion, these findings suggested that SFN protected against I/R‑induced lung lesions in rats via activation of the Nrf2/HO‑1 pathway and the accompanied anti‑inflammatory and anti‑apoptotic effects.