To investigate the protective effect of TLJN on oxygen-glucose deprivation (OGD) induced-injury of brain microvascular endothelial cells (BMECs).
The model of OGD was established in the primarily cultured BMECs. TLJN was added to the OGD-injured BMECs for 6 h. A series of assays were used to detect the effects of TLJN on: (i) MIP-1尾 content in BMECs conditioned media (CM) by ELISA; (ii) MIP-1尾 protein expression in BMECs by western blotting and immunocytochemistry; (iii) the expression of CCR5, receptor of MIP-1尾, in BMECs by western blotting; (iv) the proliferative activity of microglial cells via the Cell Counting Kit-8 (CCK-8).
Our results showed that the OGD-injured BMECs presented with large amounts of secretion and expression of MIP-1尾 and up-regulation of CCR5. Also, the CM of OGD-injured BMECs remarkably increased the proliferative activity of microglial cells. The TLJN-treated BMECs exhibited a reduction of MIP-1尾 content in BMECs-CM and a down-regulation of MIP-1尾 and CCR5 expression. In addition, an inhibitory effect of CM of OGD-injured plus TLJN injection-treated BMECs on microglial proliferation was also found.
TLJN reduced the expression of MIP-1尾 and CCR5 in OGD-injured BMECs, and the CM of OGD-injured plus TLJN injection-treated BMECs inhibited the proliferative activity of microglial cells, suggesting the therapeutic potential of TLJN on ischemic cerebral vascular disease.