| Purpose To observe treatment of Tanshinone IIA, and mixture of Tanshinone IIA and salvianolic acid B in different proportions in the brain artery occlusion rat model of ischemic tissue on Glial fibrillary acidic protein (Glial fibrillary acidic protein, GFAP) and Glial cell line-derived neurotrophic factor (Glial cell line-derived neurotrophic factor, GDNF) and to explore the mechanism of neuroprotection in cerebral ischemia and reperfusion.Methods Focal cerebral ischemia-reperfusion injury model was induced by middle cerebral artery occlusion in Sprague-Dawley rats. Using HE staining and immunohistochemical methods to observe the pathological changes of ischemic brain tissue and the expression of the Glial fibrillary acidic protein and the Glial cell line-derived neurotrophic factorResult HE staining result show neuron cell necrosis in model group is the most obvious and visible nuclear condensation,fragmentation, Tissue necrosis of the medication treatment group is less serious compared with the model group. For the sham group and blank group, the nuclei is complete with clear nucleolus, cytoplasm is lightly stained and the boundary of cells and mesenchyme. Compare with the Tanshinone IIA group, the groups treated by mixture of Tanshinone IIA and salvianolic acid B indifferent proportions have lighter necrosis, the most obvious one is the TsnIIA30/SAB300group.In rats with cerebral ischemia injury after24h and48h two time points, compared with the same time of the TsnIIA group, the increasing of GFAP in TsnIIA30/SAB100group is more difference24h after I/R, with TsnIIA30/SAB100group as the most difference one48h after I/R. Compared with the same time of the TsnIIA group, the increasing of GFAP in TsnIIA30/SAB300group has highly significant difference24h and48h after I/R. Compared with the same T of the TsnIIA30/SAB100group, the expression of GFAP in TsnIIA30/SAB300group has highly significant difference. In rats with cerebral ischemia injury after24h and48h two time points Compared with the same time of model group, the medication group increase the expression of GDNF. Compared with the same time of the TsnIIA group, the expression of GDNF increase in TsnIIA30/SAB100group has highly significant difference24h after I/R, but, with TsnIIA30/SAB100group as no difference one48h after I/R. Compared with the same time of the TsnIIA group, the increasing of GDNF in TsnIIA30/SAB300group is highly significant difference24h and48h after I/R. Compared with the same time of the TsnIIA30/SAB100group, the expression of GDNF in TsnIIA30/SAB300group has highly significant difference.Conclusion Tsn IIA and the mixture of different proportions of TsnIIA/SAB can increase the expression of GFAP and GDNF, so that activate glial cell, in order to improve the pathologic tissue of focal cerebral ischemia-reperfusion (I/R). Tsn IIA can increase the expression of GFAP and GDNF, thus, it may cooperate with salvianolic acid B to reach the synergy on increasing GFAP and GDNF. The effect is more obvious with salvianolic acid B ratio increase, it is dose-response relationship with salvianolic acid B. The mixture of different proportions of TsnIIA/SAB has a certain timeliness on GDNF expression.The positive synergistic effect with the mixture on activation of glial cells is better than TsnIIA. |
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