动物实验 z-bo 2020-08-21 552

　　Objective: To investigate the effect of 17βestradiol on the apoptosis of primary cultured cortical neurons induced by propofol and its mechanism.

　　Methods: Rat cortical neurons cultured for 7 days were randomly divided into 3 groups: solvent control group (20% fat emulsion in a different solvent), propofol group (propofol final concentration of 500μmol/L) . 17β estradiol + propofol group (the final concentration of 17β estradiol is 0.1μmol/L, the final concentration of propofol is 500μmol/L). After treating cortical neurons with the above drugs for 12 hours, Hoechst 33258 nuclear staining and TUNEL method were used to detect the apoptosis of cortical neurons, and Western blotting was used to detect neuronal Bcl-2 and Bax and to measure the level of cleaved caspase-3 protein.

　　Results: Compared with the solvent control group, the apoptosis rate of neurons in the propofol group was significantly increased (P\u003c0.01), the Bcl-2 protein level was significantly reduced (P\u003c0.01), and the Bax protein level was significantly increased. Significantly increased (P\u003c0.01), Bcl-2/Bax significantly decreased (P\u003c0.01), and cleavedcaspase-3 protein level was significantly increased (P\u003c0). .01). Compared with the propofol group, the apoptosis rate of neurons in the 17β estradiol + propofol group was significantly reduced (P\u003c0.01), and the Bcl-2 protein level was significantly increased (P\u003c0.01), and The protein level of Bax decreased significantly (P\u003c0.01), Bcl-2/Bax increased significantly (P\u003c0.01), and the protein level of cleavedcaspase-3 decreased significantly (P\u003c0). .01).

　　Conclusion: 17β estradiol exerts a protective effect by influencing the levels of Bc1-2 and Bax protein to inhibit cortical neuron apoptosis.