Sulforaphane attenuates renal ischemia reperfusion injury in mice by Nrf-2 against inflammation / 西安交通大学学报(医学版)

ABSTRACT

Objective: To explore the effect and mechanism of sulforaphane on renal ischemia reperfusion injury (IRI) in mice to provide experimental evidence for effective intervention in renal IRI. Methods: Totally 24 male C57 mice were randomly divided into four groups control group (Ctrl), IRI group, sulforaphane intervention IRI group (IRI + SFN), and sulforaphane alone group (SFN). SFN was injected into the mice at the dosage of 500 μg/kg 24 h before surgery. The renal IRI model was established by using the bilateral renal pedicles of mice with non-invasive vascular clamping for 45 min. After 24 h of renal blood perfusion, we sacrificed the mice and collected the whole blood and kidney tissue samples for pathological and biological examinations. The levels of TNF-α, IL-1β and IL-6 in murine serum were tested by ELISA. The expression levels of Nrf-2, keap-1, p-iκBα, IκBα and NFκB p-p65 in murine kidney were detected by Western blot. Results: Sulforaphane could improve renal function in mice with ischemia reperfusion and reduce apoptosis of renal tubular epithelial cells. Sulforaphane could also decrease the levels of TNF-α, IL-1β and IL-6 in murine serum and increase the expression of Nrf-2 in murine kidney tissue after ischemia reperfusion. Moreover, sulforaphane decreased the expression of p-iκBα in total protein and NFκB p-p65 in nucleus protein of renal tissue. Conclusion: Sulforaphane could inhibit phosphorylation, thus inhibiting the phosphorylation of NFκB p65 to translocation into the nucleus. Further it prevented the expressions of downstream inflammatory factors such as TNF-α, IL-1β and IL-6. Finally sulforaphane attenuated renal IRI in mice by Nrf-2 against inflammation.