Both TLR4 and TLR2 participated in the mediation of the inflammatory injury in the process of partial cerebral ischemia/reperfusion.However,it still remains unclear whether a crosstalk exists between TLR2 and TLR4 in ischemic cerebral damage.In the present study,we investigated the effect of TLR4 signaling on TLR2 expression during mimic cerebral I/R in vitro.BV-2 cells were cultured and treated with ischemia/reperfusion,then transfected with the plasmid pEGFP-H1/TLR4-siRNA,the plasmid pEGFP-H1/control sequence-siRNA and the blank plasmid,respectively.Interestingly,the expression of TLR2 and TLR4 mRNA and protein,NF-κB p65 mRNA and supernatant TNF-α level were significantly higher in ischemia/reperfusion treated cells than those lack of ischemia/reperfusion treatment,and as compared with those in ischemia/reperfusion treated cells without transfection,no significant differences about the above mentioned gene and protein expression were found in the blank plasmid tranfected cells and the plasmid pEGFP-H1/control sequence-siRNA transfected cells respectively,while the expression levels in the plasmid pEGFP-H1/TLR4-siRNA transfected cells were significantly lower.Additionally,in order to determine the effects of pyrrolidinediethyldithiocarbamate (PDTC),an NF-κB inhibitor,on the TLR4-induced TLR2 expression in BV-2 cells treated with ischemia/reperfusion,it was found that TLR4 and TLR2 mRNA expressions in PDTC pretreated cells were significantly lower in comparison with normal saline pretreated cells and non-pretreated cells.The data suggested that TLR2 activation,signaled by TLR4 and regulated by NF-κB,might be directly involved play an important role in ischemia/reperfusion induced brain damage. Both TLR4 and TLR2 participated in the mediation of the inflammatory injury in the process of partial cerebral ischemia / reperfusion. However, it still remains unclear whether a crosstalk exists between TLR2 and TLR4 in ischemic cerebral damage. In the present study, we investigated the effect of TLR4 signaling on TLR2 expression during mimic cerebral I / R in vitro.BV-2 cells were cultured and treated with ischemia / reperfusion, then transfected with the plasmid pEGFP-H1 / TLR4-siRNA, the plasmid pEGFP-H1 / control sequence- siRNA and the blank plasmids, respectively. Interestingly, the expression of TLR2 and TLR4 mRNA and protein, NF-κB p65 mRNA and supernatant TNF-α levels were significantly higher in ischemia / reperfusion treated cells than those lack of ischemia / reperfusion treatment, and as compared with those in ischemia / reperfusion treated cells without transfection, no significant differences about the above mentioned gene and protein expression were found in the blank plasmid tranfected cells and the plasmid pEGFP-H1 / control sequence-siRNA transfected cells respectively, while the expression levels in the plasmid pEGFP-H1 / TLR4-siRNA transfected cells were significantly lower. Additionally, in order to determine the effects of pyrrolidinediethyldithiocarbamate (PDTC), an NF -κB inhibitor, on the TLR4-induced TLR2 expression in BV-2 cells treated with ischemia / reperfusion, it was found that TLR4 and TLR2 mRNA expressions in PDTC pretreated cells were significantly lower in comparison with normal saline pretreated cells and non-pretreated cells The data suggested that TLR2 activation, signaled by TLR4 and regulated by NF-κB, might be directly involved in play an important role in ischemia / reperfusion induced brain damage.