YC-1 reduces inflammatory responses by inhibiting nuclear factor-κB translocation in mice subjected to transient focal cerebral ischemia

3-(5-hydroxymethyl-2-furyl)-1-benzyl-indazole (YC-1) is understood to protect against ischemic stroke, but the molecular basis for its neuroprotection remains to be fully characterized. The present study investigated the influence of YC-1 on inflammatory responses following experimental stroke. Previous studies indicated that nuclear factor (NF)-κB-driven signals serve a pivotal role in mediating inflammatory responses following stroke. Ischemic stroke results in activation of NF-κB to induce gene expression of factors including inducible nitric oxide synthase, interleukin (IL)-1β, IL-6 and matrix metalloproteinases (MMPs). The results of the present study demonstrated that YC-1 effectively reduced brain infarction and brain edema, and improved blood-brain barrier leakage. Additionally, animals treated with YC-1 exhibited significant reductions in neutrophil and macrophage infiltration into the ischemic brain. Furthermore, YC-1 effectively inhibited NF-κB translocation and binding activity, and the activity and expression of MMP-9 following ischemic stroke. In conclusion, YC-1 may effectively attenuate NF-κB-induced inflammatory damage following cerebral ischemia-reperfusion.