Protective Effect Of Ginkgolide B On Methamphetamine Induced TLR4-NF-?B Pathway Activation In BV2 Cells

Accumulating evidence suggests that microglial cells have altered morphology and proliferation in different brain regions of methamphetamine(Meth)abusers and Meth-abusing animal models.However,the possible mechanisms underlying Meth-induced microglial activation remain poorly understood.Meanwhile,Toll-like receptor4(TLR4)is closely associated with inflammation.Ginkgolide B(GB)is a diterpene lactone extracted from Ginkgo biloba.Therefore,we explored whether Meth treatment affects TLR4 expression;in addition,we evaluated the effects of ginkgolide B(GB)on Meth-mediated inflammation.BV2 cells were treated with Meth.Interestingly,Meth treatment significantly increased TLR4 expression,activated the NF-?B signaling pathway,and promoted TNF-?,IL-6 and IL-1?excretion.The siRNA technology was applied to knock down TLR4,which resulted in hampered Meth-mediated inflammatory responses,confirming the important role of TLR4 in this process.In addition,we also found that ginkgolide B can attenuate the expression of TLR4 and NF-?B and the secretion of inflammatory cytokines.Taken together,our findings revealed that Meth exposure results in BV2 cell activation,in association with TLR4-NF-kB upregulation.GB could attenuate Meth-induced inflammation,at least partially through TLR4-NF-?B signaling pathway.