Salidroside attenuates dextran sulfate sodium-induced colitis in mice via SIRT1/FoxOs signaling pathway.

Salidroside (Sal), the active ingredient of Rhodiola rosea L, has various pharmacological activities, including antioxidant, anti-inflammatory and anti-tumor activities. Recently, studies have shown that oxidative stress and apoptosis are related to the pathogenesis of inflammatory bowel disease. Therefore, we evaluated the effects of Sal on oxidative stress and apoptosis in colitis mice through the SIRT1/FoxOs pathway. To induce the colitis model, mice continuously consumed water containing 3% DSS for 7 days; some mice were also treated with Sal and the SIRT1/FoxOs pathway blocker selisistat (Ex527). Changes in body weight, DAI, colon length and colon tissue histology as well as SOD, GSH-Px and CAT activities were measured. The expression of SIRT1, FoxO1, FoxO3a, FoxO4, caspase-3, cleaved-caspase-3, Bax and Bcl-2 in colorectal tissues was detected by RT-PCR and Western blotting. The study showed that Sal decreased the DAI score, weight loss, colon shortening and colon tissue damage in colitis mice. Sal inhibited oxidative stress by upregulating SOD, GSH-Px and CAT while suppressing colonic apoptosis by downregulating the expression of Bax, caspase-3, and cleaved-caspase-3 and upregulating the expression of Bcl-2. Sal also activated SIRT1/FoxOs signaling, which increased the expression of SIRT1, FoxO1, FoxO3a and FoxO4 in colon tissue. Furthermore, SIRT1/FoxOs pathway inhibition using Ex527 partially eliminated the effect of Sal on colitis mice. The study manifested that Sal may protect colitis mice by activating the SIRT1/FoxOs pathway, which is related to oxidative stress and apoptosis in colon tissues.