Nephroprotective Effects of N-Acetylcysteine Amide against Contrast-Induced Nephropathy through Upregulating Thioredoxin-1, Inhibiting ASK1/p38MAPK Pathway, and Suppressing Oxidative Stress and Apoptosis in Rats

Figure 6

Schematic diagram illustrates the signal mechanism for CIN and the renoprotection of NACA. Contrast media exposure increases ROS production in kidney, resulting in suppression of Trx1 and thus dissociating the Trx1/ASK1 complex to facilitate the activation of ASK1 (phosphorylation). Subsequently, activated ASK1 results in the downstream activation of its substrate p38 MAPK, an imbalance of pro- and antiapoptotic members of the Bcl-2 family, and finally induces apoptosis. NACA efficiently inhibits such a pathologic process through its antioxidant activity and by upregulating Trx1. p, phosphorylation. Ps, phosphatidylserine.