Effect of magnolol on hippocampal neuroplasticity in unpredictable chronic mild stress treated rats / 中草药

ABSTRACT

Objective To investigate the effect and mechanism of magnolol on hippocampal neuroplasticity in depression model rats. Methods In this study, depression model rats were prepared with unpredictable chronic mild stress (UCMS), and was given different doses of magnolol (20, 40 mg/kg) for 28 d. The rats in the positive control group were given fluoxetine (20 mg/kg) for 28 d. The ameliorative effects of magnolol on symptom of depression were investigated through behavior tests including open-field test, sucrose preference test, and forced-swimming test. The mRNA levels of Map-2, Gap43, and SYP in the hippocampus, cortex and striatum of rats in each group were detected by qRT-PCR, and the localization and expression of MAP-2, GAP43, and SYP in the hippocampus were observed by immunohistochemical staining analysis. The quantitative analysis of MAP-2, p-MAP-2, and p-ERK in hippocampus of rats in each group were further analyzed by Western blotting. Results UCMS was able to decrease the sucrose preference index, reduce locomotor activity and increase the immobility time in the forced swimming test. Compared with model group, magnolol significantly increased the spontaneous activity of rats, increased the consumption of sugar and water, and decreased the immobility time of chronic stress rats in forced swimming (P < 0.05, 0.01). Magnolol reversed MAP-2 mRNA and protein level in the hippocampus, increased phosphorylated MAP-2 expression in the hippocampus (P < 0.05), and significantly restored the p-ERK expression (P < 0.05). Conclusion Magnolol can affect the phosphorylation of MAP-2 through ERK pathway and increase the expression of MAP-2, thus affecting the neuronal plasticity and exerting its antidepressant effect.