[No authors listed]
Abnormal blood-brain barrier (BBB) is a common pathological feature in brain damage. In the present study, a brain microvascular endothelial cell (BMEC) model was established to determine the role of the tollâlike receptor 4 (TLR4)/protein kinase Cα signaling pathway in BBB dysfunction. Three small interfering (si)RNAs directed against were designed to investigate the molecular mechanisms of duanyu1531α underlying BBB damage. BMECs were divided into 4 groups: Control group, TAKâ242 (a TLR4 inhibitor) group, group and group. The results indicated that siRNAâ3 was the most effective at silencing duanyu1531α gene expression. Reverse transcriptionâquantitative polymerase chain reaction (RTâqPCR) analysis indicated no significant difference of TLR4 mRNA expression levels between three different treated groups and the Control group. However, duanyu1531α mRNA expression in the duanyu1531αâsiRNA and TAKâ242+duanyu1531αâsiRNA groups were significantly decreased compared with that in Control and TAKâ242 groups. In addition, occludin mRNA expression in duanyu1531αâsiRNA and TAKâ242+duanyu1531αâsiRNA groups were significantly higher compared with the Control group. Meanwhile, occluding expressions in three treated groups were also significantly higher compared with the Control group. Furthermore, TAKâ242 treatment, duanyu1531αâsiRNA treatment, and TAKâ242+duanyu1531αâsiRNA treatment could promote occludin junctional labeling compared with the Control group. The permeability of duanyu1531αâsiRNA and TAKâ242+duanyu1531αâsiRNA groups was significantly promoted compared with the control group. The signaling pathway was closely related to BBB damage. The present study will lead to an improved molecular understanding of BBB damage in the future.
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