Fig. 7

Working model of the molecular mechanisms by which NOD1/RIP2 signalling mediates the ICH-induced inflammatory response and undergoes positive crosstalk with inflammatory factors during ICH in mice. More specifically, ICH-induced damage-associated molecular patterns (DAMPs) were able to initiate the activation of NOD1, which then resulted in the activation of its adaptor RIP2. Activated RIP2 in turn exerted its regulatory effect on the proinflammatory factors TNF-α and IL-1β via JNK/P38 MAPK- and NF-κB-dependent signalling, and the proinflammatory factors TNF-α and IL-1β that were induced by NOD1/RIP2 signalling also enhanced NOD1/RIP2 upregulation. Either the NOD1 inhibitor ML130 or RIP2 inhibitor GSK583 could suppress the inflammatory response induced by ICH. The P38 inhibitor SB202190, JNK inhibitor SP600125, and NF-κB inhibitor BAY11-7082 were used for intervention