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.
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