Fig. 9.

Schematic depiction of the modified Alb and its role as well as mechanisms in the treatment of DSS colitis. (A) Reductively modified Alb and its –SH group-mediated interaction with other redox molecules. DTT treatment dramatically increases the number of –SH groups through maintaining Cys34 at the reduced state and cleaving the intra-chain disulfide bonds. The increased –SH groups in Alb react with H₂O₂, causing sulfenic acid formation (-SOH), which can be further detoxified in the presence of additional –SH groups from Alb or other small thiol antioxidant GSH. The –SH group-mediated interaction between Alb and GSH/GSSG contributes to maintaining systemic redox homeostasis. (B) Therapeutic effects of r-Alb on DSS colitis. DSS induces ROS production in intestinal epithelial cells, which results in the disassembly of adherens and tight junction, leading to bacterial invasion, recruitment of inflammatory cells, local inflammatory reactions, ROS releasing, and cell injury. R-Alb detoxifies the major oxidant H₂O₂ and subsequently attenuates ROS-induced inflammation and cell injury.