Our results showed that the repeated I3C treatment during the 10-days of defeat stress exposure suppressed the CSDS-induced increases in the mRNA and protein levels of IL-1β, IL-6, and TNF-α in the hippocampus and prefrontal cortex, suggesting that I3C supplementary may exhibit strong anti-neuroinflammatory activities in animal models of depression. The gene discussed is IL1B; the disease is major depressive disorder.