However, HBMECs were incubated with astaxanthin; cell viability was significantly increased in a concentration-dependent manner.
Effects of astaxanthin on Wnt/f)-catenin signaling pathway in HBMECs with normal oxygen and OGD
HBMECs were incubated with astaxanthin (3-30 [micro]M) for 24 h robustly leading to a rapid reduce in p-GSK3[beta], and increase wnt7a, [beta]-catenin, cyclin D1 expression, as shown in Fig.
HBMECs were incubated with astaxanthin 10 [micro]M for 24 h in 24-well plates in serum-free media previously coated with growth factor-reduced matrigel matrix, and then IWR-1-endo with 5 [micro]M continue to develop 8 h.
HBMECs were incubated with astaxanthin 10 [micro]M for 24 h, and then IWR-1-endo with 5 [micro]M continue to cultivate 8 h, robustly activated Wnt/[beta]-catenin signaling pathway, leading to a rapid increase in P-GSK3[beta], reduce the wnt7a, [beta]-catenin and cyclin D1 expression, as shown in Fig.
The major finding of the present study is that astaxanthin induce proliferation, migration and tube formation in HBMECs and RASMCs in vitro.
When different concentrations of astaxanthin cultivate HBMECs and RASMCs, the expression of p-GSK3[beta] decreased obviously, while [beta]-catenin expression increased significantly.
In our study, astaxanthin up-regulated [beta]-catenin expression in HBMECs and RASMCs, the major effects of astaxanthin appeared to take place via anti-phosphorylation rather than absolute alterations of protein levels.
The results showed that oxygen glucose deprivation increased Caspase-3 activity in cultured HBMECs.