17β-estradiol protects cortical neurons from propofol-induced apoptosis by activating PI3K-Akt signaling pathway

AIM: To investigate the protective effects and the mechanisms of 17β-estradiol on the propofol-induced neuroapoptosis in primary cultured cortical neurons. METHODS: The neurons were cultured for 7 d and treated with different concentrations of propofol and/or 17β-estradiol, respectively. The neuron viability, neuroapoptosis and the protein level of p-Akt was determined by MTT assay, Hoechst 33258 staining and Western blot 12 h after different treatments, respectively. RESULTS: Compared with vehicle-control group, propfol inhibited neuron viability in a dose-dependent manner (P<0.05). Compared with propofol treatment group, 17β-estradiol increased the neuron viability in a dose-dependent manner (P<0.05), and IGF increased the neuron viability greatly (P<0.01). Compared with vehicle-control group, the number of apoptotic neurons which was significantly decreased by treatment of 17β-estradiol was markedly increased by propofol (P<0.01). Compared with the 17β-estradiol+propofol group, LY294002 increased the number of apoptotic neurons (P<0.01). Compared with vehicle-control group, propfol decreased the protein level of p-Akt in a dose-dependent manner (P<0.05). Compared with propofol treatment group, 17β-estradiol increased the protein level of p-Akt in a dose-dependent manner (P<0.05). Compared with 17β-estradiol+propofol group, LY294002 significantly decreased the protein level of p-Akt (P<0.01). CONCLUSION: 17β-estradiol exerts the neuroprotective effects against propofol-induced neuroapoptosis by activating the PI3K-Akt signaling pathway.