Sulforaphane alleviates hepatic ischemia-reperfusion injury through promoting the activation of Nrf-2/HO-1 signaling.

Abstract Background Sulforaphane (SFN)displays both anti-oxidative stress and anti-inflammatory activity. Given that inflammation and oxidative stress play important roles in hepatic ischemia-reperfusion injury (HI/RI), we examined the protective effect and potential mechanism of SFN on HI/RI. Methods The maneuver of Pringle's was used to establish the mode of HI/RI and 60 SD rats were randomly divided into Sham, HI/RI, SFN and ML385 Groups. The expression of aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), Nuclear factor-E2-related factor 2(Nrf-2), heme oxygenase 1(HO-1), nitric oxide (NO), Cyclooxygenase2 (COX-2), NADPH quinone oxidoreductase 1 (NQO1), malondialdehyde (MDA), tumor necrosis factor-a (TNF-a), interleukin-6 (IL-6) and monocyte chemotactic protein 1(MCP-1) were measured. Moreover, hepatic pathological morphology and the activity of glutathione (GSH), Catalase (CAT), superoxide dismutase (SOD) of the liver were also examined. Results SFN treatment can significantly decrease the hepatic pathological injury and down-regulate the expression of ALT, AST, ALP, COX-2, TNF-a, IL-6, MCP-1, NO and MDA in HI/RI with increasing the expression of Nrf2, NQO1 and HO-1, and up-regulating the activity of GSH, CAT and SOD. Moreover, Nrf-2 inhibitor, ML385 can obliviously reverse the protective effect of SFN on HI/RI. Conclusion Sulforaphane can inhibit the inflammatory response and oxidative stress induced by HI/RI through promoting the activation of the Nrf-2 / HO-1 signal pathway.