Background It has been known that platelet activating factor receptors(PAFR)may mediate many acute pathologicalresponses and that PAFR antagonist Ginkgolide B(GB)possesses multiple effects,but the actions of GB on PAFR affinity andmitochondrial respiration in the ischemic neuron were unclear until now.This study explored the possible effects of GB on PAFRand the mitochondrial respiration of the neuron in the ischemic microenvironment.Methods Thrombotic cerebral ischemia in tree shrews was induced by a photochemical reaction;changes in the regionalcerebral blood flow(rCBF,using ~(99m)TC tracer technique),the brain water content(specific gravimetric method),PAFR(3H-labelled PAF assay),the respiratory control rate(RCR),the phosphorus-oxygen(P/O)ratio of mitochondrial respiration(Clark oxygen electrode),mitochondrial permeability transition(MPT)pore,and the mitochondrial ultrastructure in the ischemicneurons were also observed.Data were compared between the two groups(the ischemia group vs the sham group,and theischemia group vs the GB group).Results There were high affinity and low affinity sites for PAFR on the tree threws’ brain cell membranes.The varying-affinityPAFR binding sites,the respiration state Ⅲ,the state Ⅳ,RCR,the P/O ratio of the mitochondria,and the rCBF all decreasedmarkedly(respectively,P<0.01 and P<0.05),but the water content increased(P<0.01)in the ischemia group after the applicationof cerebral thrombosis.In tree shrews treated with GB(5 mg/kg i.v.)6 hours after photochemical reaction,their PAFR bindingsites and respiratory state increased markedly.The rCBF gradually increased and the brain edema ameliorated(P<0.01)at 24hafter cerebral ischemia.There were significant differences between the ischemia group and sham group(P<0.01).In GB treatedisolated neurons’ mitochondria,with or without cerebral ischemia,the energy metabolism of the mitochondria had not beenchanged.Conclusions The activation of the PAFR may play an important role in the inhibition of the mitochondrial respiration and theinduction of neuronal damage after cerebral thrombosis;however,GB possesses neuroprotective effects by improvingmitochondrial metabolism.Chin Med J 2007;120(17):1529-1533 Background It has been known that platelet activating factor receptors(PAFR) may mediate many acute pathologicalresponses and that PAFR antagonist Ginkgolide B(GB)possesses multiple effects,but the actions of GB on PAFR affinity and mitochondrial respiration in the ischemic neuron were unclear until now. This study explored the possible effects of GB on PAFRand the mitochondrial respiration of the neuron in the ischemic microenvironment.Methods Thrombotic cerebral ischemia in tree shrews was induced by a photochemical reaction;changes in the regionalcerebral blood flow(rCBF,using ~(99m)TC Tracer technique), the brain water content (specific gravimetric method), PAFR (3H-labelled PAF assay), the respiratory control rate (RCR), the phosphorus-oxygen (P/O) ratio of mitochondrial respiration (Clark oxygen electrode), Mitochondrial permeability transition(MPT)pore,and the mitochondrial ultrastructure in the ischemicneurons were also observed.Data were compared between the two groups(the The sham group, and theischemia group vs the GB group).Results There were high affinity and low affinity sites for PAFR on the tree threws’ brain cell membranes.The varying-affinityPAFR binding sites,the respiration state III,the state IV,RCR ,the P/O ratio of the mitochondria,and the rCBF all decreasedmarkedly (respectively,P<0.01 and P<0.05),but the water content increased (P<0.01) in the ischemia group after the application of cerebral thrombosis.In tree shrews After treatment with GB (5 mg/kg iv) 6 hours after photochemical reaction, its PAFR binding sites and respiratory state eviction markedly. The rCBF gradually increased and the brain edema ameliorated (P<0.01) at 24hafter cerebral ischemia. There were significant differences between the In the group of HGH group and sham (P<0.01).In GB treated isolated neurons’ mitochondria,with or without cerebral ischemia,the energy metabolism of the mitochondria had not been changed.Conclusions The activation of the PAFR may play an important role in the inhibiti OnOf the mitochondrial respiration and theinduction of neuronal damage after cerebral thrombosis;however,GB possesses neuroprotective effects by improvingmitochondrial metabolism.Chin Med J 2007;120(17):1529-1533