Ginsenoside Rb1 improve cerebral ischemia-reperfusion induced blood-brain barrier injury in mice by regulating MAPK pathway
Objective To explore the effects and underlying mechanisms of ginsenoside Rb,(Rb1)on the blood-brain barrier(BBB)injury induced by cerebral ischemia reperfusion in mice.Methods C57BL/6J mice were randomly divided into sham operated group,model group,low,medium,high dose group of Rb,(5,10,and 20 mg·kg-1).This research used the middle cerebral artery occlusion and reperfusion(MCAO/R)animal model.After 1 h of ischemia and 24 h reperfusion,brain tissues of mice were extracted from executed mice.The evaluation of BBB damage in each group of mice was measured using Evans blue staining.The mRNA expression levels of the inflammatory factors—interleukin-1β(IL-1β),interleukin-6(IL-6)and tumor necrosis factor-α(TNF-α),as well as the expression of Zonula occludens-1(ZO-1)and Occludin were examined in the brain tissues of mice by the qRT-PCR.Western blotting method was uesd to detect the expression levels of ZO-1,Occludin,Matrix metalloproteinase-2/9(MMP-2/9),and MAPK related proteins in the brain tissue of each group of mice.Results Compared with the model group,Rb,significantly reduced the leakage of Evans blue in brain tissue of mice with cerebral ischemia-reperfusion(P＜0.05),and significantly reduced the mRNA transcription level of IL-1β,IL-6 and TNF-α in brain tissue(P＜0.05,0.01),significantly upregulated the mRNA transcription and protein expression levels of ZO-1 and Occludin(P＜0.05,0.01),significantly reduced the protein expression levels of MMP-2 and MMP-9(P＜0.05,0.01),significantly inhibited the expression of phosphorylated proteins p38,JNK,and ERK in the MAPK pathway (P ＜ 0.05, 0.01). Conclusion Rb, can ameliorate BBB damage via inhibiting the activation of MAPK signal pathway, down-regulate the expression of MMP-2 and MMP-9, attenuate the degradation of ZO-1 and Occludin in MCAO/R-induced mice.
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