Salvianolic acid B ameliorates neuroinflammation and neuronal injury via blocking NLRP3 inflammasome and promoting SIRT1 in experimental subarachnoid hemorrhage

The nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin containing 3 (NLRP3) inflammasome-mediated immuno-inflammatory response plays a critical role in exacerbating early brain injury (EBI) after subarachnoid hemorrhage (SAH). Salvianolic acid B (SalB) has previously been shown to suppress neuroinflammatory responses many disorders. Meanwhile, previous study demonstrated that SalB mitigated oxidative damage and neuronal degeneration prechiasmatic injection model of SAH. However, the therapeutic potential on SAH remains unclear. In present study, we explored effects an endovascular perforation model. We observed ameliorated SAH-induced functional deficits. Additionally, significantly microglial activation, pro-inflammatory cytokines release, injury. Mechanistically, inhibited NLRP3 inflammasome activation increased sirtuin 1 (SIRT1) expression Administration EX527, inhibitor SIRT1, abrogated anti-inflammatory against further induced activation. contrast, MCC950, potent selective inhibitor, reversed detrimental SIRT1 inhibition by EX527 EBI. These results indicated effectively repressed action appeared be mediated blocking promoting signaling.