Beneficial effects of chlorogenic acid treatment on neuroinflammation after deep hypothermic circulatory arrest may be mediated through CYLD/NF-κB signaling

The modulation of TRAF6 and RIP1 ubiquitination by CYLD participates in the negative regulation of NF-κB pathway treated with CA after DHCA. After DHCA, the inflammatory molecules, TNF-α, IL-6 and IL-1β are increased, and the canonical pathway of NF-κB is activated. The TRAF6 and RIP1 are key proteins for NF-κB activation which exhibit ubiquitin ligase activity. CA treatment up-regulates CYLD expression, and then CYLD modulates K48/K63 chains ubiquitination on TRAF6 and RIP1 to suppress NF-κB signalling.