Figure 9.

Schematic diagram illustrating the possible negative feedback loop mechanism between A20/TRAF6/NF-κB signaling after SAH. (A) Under the SAH conditions, inhibition of NF-κB by injection of TPCA-1 caused a reduction in inflammatory cytokine IL-6, IL-1β, and TNF-α release, and A20 expression was suppressed, which increased the expression of TRAF6. When A20 was inhibited by lentivirus, the expression levels of TRAF6 and NF-κB both increased, causing aggravation of the inflammatory response. Meanwhile, lentivirus-mediated overexpression of A20 decreased the release of inflammatory cytokines by suppressing TRAF6 and NF-κB. (B) As illustrated, the expression of A20 was regulated by NF-κB. In turn, the increased expression of A20 inhibited TRAF6 and NF-κB expression to reduce the subsequent inflammatory response and exert neuroprotective effects.