PROTECTIVE EFFECT AND MECHANISM OF PROPOFOL ON CONDENSED AΒ25-35-INDUCED INJURY OF RAT HIPPOCAMPAL NEURONS

Shudong Yao, Xiaoling Shi1, Wei Jia^*

Department of Anesthesiology, Huangshi Central Hospital (Affiliated Hospital of Hubei Polytechnic University), Edong Healthcare Group, Huangshi, PR China

Objective: To investigate the protective effect and mechanism of propofol on on rat hippocampal neurons that have endured condensed Aβ25-35-induced injuries.

Methods: Twelve newborn rats were collected, and 12 rat hippocampal neuronal cells were taken as a control group without any treatment; the remaining rat hippocampal neuronal cells were randomly divided into an Aβ_25-35 group and a propofol group, 12 each. Both groups were induced by 10μmol/L Aβ_25-35 to establish a cell injury model. The Aβ_25-35 group was not treated and the propofol group was treated with 20μmol/L propofol After the effect was over, experiments were carried out comparing the survival rate of rat hippocampal neurons, apoptosis-related proteins (Bcl-2, Bax), Tau protein phosphorylated proteins (p-Tau Ser404, p-Tau Ser396, p-Tau Thr231) and glycogen synthase kinase 3β (glycogen synthetase kinase 3 β, GSK3β) protein expression level.

Results: The survival rate and apoptosis rate of hippocampal neurons in the Aβ_25-35 group were significantly lower than those in the control group (p<0.05). The survival rate and apoptosis rate of hippocampal neurons in the propofol group were significantly higher than those in the control group (p<0.05). The expression level of Bax in hippocampal neurons of the Aβ_25-35 group was significantly higher than those of the control group, and the expression of Bcl-2 and apoptosis rate were significantly lower than those of the control group (p<0.05). The expression level of Bax in hippocampal neuron cells of the propofol group was significantly lower than that of control group, and the expression of Bcl-2 and apoptosis rate were significantly higher than that of control group (p<0.05). The expression levels of p-Tau Ser404, p-Tau Ser396, and p-Tau Thr231 in hippocampal neurons of the Aβ_25-35 group were significantly higher than those in the control group (p<0.05). The expression levels of p-Tau Ser404, p-Tau Ser396, and p-Tau Thr231 in hippocampal neurons of the propofol group were significantly lower than those in the Aβ_25-35 group (p<0.05). There was no statistically significant difference in the total Tau protein expression level among the groups (P>0.05). The expression level of GSK-3β protein in hippocampal neurons of the Aβ_25-35 group was significantly higher than that of control group (p<0.05). The expression level of GSK-3β protein in the propofol group was significantly lower than that in the model group (P<0.05).

Conclusion: Propofol can protect rat hippocampal neuronal cells from damage induced by condensed Aβ_25-35, and propofol's mechanism may be achieved by blocking apoptosis and inhibiting GSK-3β kinase expression and Tau phosphorylation.