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Previous studies could not explain the paradox between the poor brain distribution and powerful neuroprotective effects of tanshinone ⅡA.We hypothesized in this study that the increased transport through and its direct protective effect of against the damaged blood brain barrier (BBB) might be the underlying mechanisms for the powerful neuroprotective effects of tanshione ⅡA.This study was thus designed to characterize the transport of tanshinone ⅡA through both normal and hydrogen peroxide damaged BBB,and to explore its direct protective effect on oxidative stress triggered BBB damage in an in vitro BBB model developed from the primarily cultured rat brain microvascular endothelial cells.Uptake of tanshinone ⅡA was liner over a concentration range of 4 to 40 μM.BSA addition significantly inhibited the tanshinone ⅡA uptake when terminated at 2 h.However,dynamic study showed that BSA promoted the uptake at early phase (before 1 h) while inhibited it 1 h later.