17β雌二醇 z-bo 2020-11-10 330

　　Objective: To investigate the effect and mechanism of 17β estradiol on propofol-induced apoptosis of primary cultured cortical neurons.

　　Methods: Primary cultured rat cortical neurons for 7 days were randomly divided into three groups: solvent control group (given isosolvent 20% fat emulsion), propofol group (propofol final concentration 500μmol/L), 17β estrogen Glycol + propofol group (final concentration of 17β estradiol is 0.1 μmol/L, final concentration of propofol is 500 μmol/L). After the above-mentioned drugs were used to treat cortical neurons for 12 hours, Hoechst 33258 nuclear staining method and TUNEL method were used to detect cortical neuron apoptosis, and Western-blot method was used to determine the levels of neuronal Bcl-2, Bax and cleaved caspase-3 proteins.

　　Results: Compared with the solvent control group, the neuronal apoptosis rate in the propofol group was significantly increased (P<0.01), the Bcl-2 protein level was significantly decreased (P<0.01), and the Bax protein level was significantly increased (P<0.01) ), Bcl-2/Bax decreased significantly (P<0.01), and cleaved caspase-3 protein levels increased significantly (P<0.01). Compared with the propofol group, the apoptosis rate of neurons in the 17β estradiol + propofol group decreased significantly (P<0.01), the level of Bcl-2 protein increased significantly (P<0.01), and the level of Bax protein decreased significantly (P<0.01), Bcl-2/Bax increased significantly (P<0.01), and cleaved caspase-3 protein level decreased significantly (P<0.01).

　　Conclusion: 17β-estradiol can inhibit cortical neuron apoptosis by affecting the levels of Bc1-2 and Bax protein, and produce a protective effect.