Abstract:

AIM: To investigate the mechanism of 17β-estradiol on the apoptosis of rat hippocampal neurons induced by propofol. METHODS: Sixty SD rats were randomly divided into 5 groups: control group (NS group), propofol group (P group) and 17β estradiol group (D1, D2 and D3 groups), with 12 rats in each group. The rats in the NS group were intraperitoneally injected with equal volume of fat emulsion. The rats in the P group were only intraperitoneally injected with propofol. The rats in the D1, D2 and D3 groups were intraperitoneally injected with 300, 600 and 900 μg/kg 17β estradiol, respectively. After 30 min, propofol was intraperitoneally injected. The respiratory rate (R0, R30, R60, R90), escape latency (TD1, TD2, TD3, TD4, TD5), hippocampal neuronal apoptosis index (AI) and cleaved caspase-3, p-p38 and p-NF-κB protein expression level were observed. RESULTS: Compared with the NS group, the respiratory rate of the rats in the P group was increased after the injection of propofol (P＜0.05). Compared with the P group, the respiratory rate of the D1, D2 and D3 groups was slower (P＜0.05). The escape latency of rats in group P was significantly longer than that in NS group (P＜0.05). The escape latency of group D1, D2 and D3 was significantly lower than that of group P (P＜0.05). The AI of the rats in the P group was significantly higher than that in the NS group, and the D1 group, the D2 group and the D3 group were significantly lower than the P group (P＜0.01). Compared with NS group, the expression of cleaved caspase-3, p-p38 and its downstream p-NF-κB increased in group P (P＜0.01). Compared with group P, group D1 and D2, D3, the expression of p-p38, cleaved caspase-3 and its downstream p-NF-κB was down-regulated (P＜0.01). CONCLUSION: 17β-estradiol can alleviate the apoptosis of rat hippocampal neurons induced by propofol, and its mechanism may be related to the inhibition of p38MAPK signaling pathway.

Key words: 17&beta, estradiol, propofol, rat, hippocampus, p38MAPK