However, pharmacological activation of thalamic HIF-1α and NLRP3 significantly eliminated the therapeutic effects of SGB on mechanical allodynia and anxiety- and depression-like behaviors following thalamic hemorrhage, which confirmed that SGB improved CPSP and comorbid anxiety and depression through inhibiting HIF-1α/NLRP3 inflammatory signaling. The gene discussed is NLRP3; the disease is depressive disorder.