动物造模 z-bio 2022-07-07 590

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

　　METHODS: Rat cortical neurons that were cultured for 7 days were randomly divided into three groups: solvent control group (administered isosolvent 20% fat emulsion), propofol group (final concentration of propofol was 500 μmol/L), 17β-estrogen Diol + propofol group (the final concentration of 17βestradiol was 0.1 μmol/L, and the final concentration of propofol was 500 μmol/L). The cortical neurons were treated with the above drugs for 12 h, and the apoptosis of cortical neurons was detected by Hoechst 33258 nuclear staining method and TUNEL method, and the levels of Bcl-2, Bax and cleaved caspase-3 proteins were detected by Western-blot method.

　　Results: Compared with the solvent control group, the apoptosis rate of neurons in the propofol group was significantly increased (P<0.01), the protein level of Bcl-2 was significantly decreased (P<0.01), and the protein level of Bax was significantly increased (P<0.01). ), Bcl-2/Bax was significantly decreased (P<0.01), and the protein level of cleaved caspase-3 was significantly increased (P<0.01). Compared with the propofol group, the apoptosis rate of neurons in the 17βestradiol + propofol group was significantly decreased (P<0.01), the protein level of Bcl-2 was significantly increased (P<0.01), and the protein level of Bax was significantly decreased (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 the apoptosis of cortical neurons by affecting the levels of Bc1-2 and Bax proteins, resulting in a protective effect.