| Objective To study effects of Tanshinone ⅡA (TanⅡA) on neural cellapoptosis and the permeability of the blood-brain barrier following cerebralischemia reperfusion (IR) injury rats, and explore the releationship betweentheirs and p38mitogen-activated protein kinase pathway.Method60SD rats were randomly divided into four groups, which weresham operated group, IR group, low dose TanⅡA treated group and high doseTan ⅡA treated group. The focal middle cerebral artery occlusion (MCAO)model was made in rats with suture-occluded method. Low dose and high dosegroups were pretreated with low and high does TanⅡA, for3d, before MCAO.After120min MCAO following24h reperfusion, We investigated theexpressions of phosphorylated p38MAPK and MMP-9in usingimmunohistochemistry technique in the frontal and parietal cortex; Neural cellapoptosis were investigated with TUNEL and HE staining; And blood-brain barrier(BBB) was investigated by the contents of evens blue (EB); The volumeof cerebral infarction was observed by TTC.Results⑴Compared with sham operated group, phosphorylatedp38MAPK and MMP-9increased in IR group; Compared with IR group, highand low dose Tan ⅡA treated groups dose-dependently decreased expression ofphosphorylated p38MAPK and MMP-9(P <0.05);⑵Compared with shamoperated group, cell apoptosis and pathomorphological change of ischemic areawere distinctly increased in IR group; Compared with that of IR group, low andhigh Tan ⅡA treated groups dose-dependently reduced neural cell apoptosisand pathomorphological change (all P<0.05);⑶Compared with sham operatedgroup, the contents of EB increased at24h of reperfusion. Compared with IRgroup, low and high Tan ⅡA treated groups dose-dependently reduced thecontents of EB (all P<0.05).Conclusion Tan ⅡA may attenuate neural cell apoptosis and reducing theexpression of MMP-9to protects blood-brain barrier by inhibiting p38mitogen-activated protein kinase pathway. |
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