Furthermore, within the TLR4 signaling pathway, the MyD88-dependent and TRIF-dependent signaling pathways are two important activators of NF-κB and the subsequent regulatory effects of NF-κB signaling.[35] As reported in a previous study, a Dioscin treatment ameliorates cerebral I/R injury by down-regulating the TLR4/MyD88 signaling pathway.[36] Interestingly, in our present study, the level of MyD88 expression was reduced by vinpocetine treatment after cerebral ischemia/reperfusion injury or OGD. The gene discussed is NFKB1; the disease is brain ischemia.