Fig. 8

Ex-4 restored the TJPs in bEnd.3 cells by decreasing astrocyte-derived VEGF-A levels through a mechanism mediated by the PLCγ/PKCα/eNOS pathway in bEnd.3 cells. a Representative western blots showing the levels of p-PLCγ, p-PKCα, and eNOS in bEnd.3 cells cultured with different ACMs. Total PLCγ, total PKCα, and GADPH were used as the loading controls. b Quantitative analyses of p-PLCγ, p-PKCα, and eNOS levels. The data are presented as the mean ± SD (n = 6). c Representative western blots showing the levels of p-AKT and p-PI3K in bEnd.3 cells cultured with different ACMs. Total PI3K and total Akt were used as the loading controls. d Quantitative analyses of p-PI3K and p-Akt levels. The data are presented as the mean ± SD (n = 6). ACM-Medium, cultured with ACM from untreated astrocytes; ACM-OGD+RO, cultured with ACM from astrocytes treated with OGD for 4 h plus RO for 24 h; ACM-OGD+RO+Ex4, cultured with ACM from astrocytes treated with OGD for 4 h plus RO for 24 h in the presence of Ex-4; ACM-OGD+RO+VI, cultured with ACM from astrocytes treated with OGD for 4 h plus RO for 24 h and the anti-VEGFR2 antibody. All bEnd.3 cell monolayers were pretreated with Ex(9-39) before culture with different ACMs. *P < 0.05 compared with the ACM-Medium group and ^#P < 0.05 compared with the ACM+OGD+RO group, ANOVA plus SNK test (b, d)