Sinomenine alleviates dextran sulfate sodium-induced colitis via the Nrf2/NQO-1 signaling pathway

Sinomenine (SIN), a pure alkaloid isolated from Sinomenium acutum, has been widely used in arthritis for its anti-inflammatory effect, but little is known about the effect of SIN on human ulcerative colitis (UC). In the present study, the effect and mechanism of SIN was examined in a dextran sulfate sodium (DSS)-induced murine colitis model, which mimics human UC. Oral administration of SIN significantly suppressed the elevated disease activity index and ameliorated colonic histological damage in a DSS-induced colitis model. Tumor necrosis factor-α, interleukin-6 and inducible nitric oxide synthase levels were also reduced as detected by reverse transcription-quantitative polymerase chain reaction. In addition, SIN reversed the decreased colon length and colonic superoxide dismutase activity. Furthermore, western blot analysis revealed that nuclear factor-erythroid 2-related factor 2 (Nrf2) and its downstream genes, heme oxygenase-1 and NADP(H) quinone oxidoreductase 1 (NQO-1), were markedly activated by SIN. The current results indicated that SIN alleviated DSS-induced colitis in mice, which may be due to its antioxidant properties and was at least in part dependent on the Nrf2/NQO-1 signaling pathway. Therefore, SIN may have potential applications as a protective drug for patients with UC.