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.
Keywords: Nrf-2/HO-1; Sulforaphane; ischemia-reperfusion injury; lung; reactive oxygen species.
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