In addition, it also improves dextran sodium sulfate (DSS)-induced colitis by upregulating catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities; decreasing myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β); and reversing the activation of the nuclear factor kappa-B (NF-κB) signaling pathway [19,20,21]. The gene discussed is CAT; the disease is colitis.