SIN reduces inflammation, oxidative stress, and renal damage in UUO mice.
SIN is an Nrf2 activator and it activates Nrf2 signaling through Keap1 degradation.
SIN inhibits the M1 and promotes the M2 polarization in macrophages.
SIN Nrf2-dependently relieves renal inflammation and NF-kB signaling.
Nrf2 is essential for SIN functions in inflammation inhibition and renoprotection.