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目的:研究厚朴酚对慢性温和刺激抑郁模型小鼠的抗抑郁作用。方法:采用悬尾实验、强迫游泳实验、开野实验、糖水偏好实验,研究厚朴酚对慢性温和刺激抑郁模型小鼠的抗抑郁作用。采用免疫组化方法检测厚朴酚对抑郁模型小鼠海马内脑源性神经营养因子(BDNF)的表达和溴脱氧脲嘧啶核苷(BrdU)掺入DNA合成的影响。结果:厚朴酚(40mg/kg)能显著增加抑郁模型小鼠的体重;厚朴酚(40mg/kg)能显著增加抑郁模型小鼠开野实验的自发活动的水平穿格次数;厚朴酚(40mg/kg)能显著缩短抑郁模型小鼠悬尾和强迫游泳不动时间;厚朴酚(40mg/kg)能显著提高抑郁模型小鼠的基础糖水偏好值。厚朴酚能促进海马神经元再生,显著增加抑郁模型小鼠海马BDNF和BrdU阳性细胞的数。结论:厚朴酚(40mg/kg)具有显著的抗抑郁作用,通过增加海马表达BDNF来促进海马神经元再生是其抗抑郁的作用机制之一。
Objective: To study the antidepressant effects of magnolol on chronic mild stress-induced depression model mice. Methods: The anti-depression effects of honokiol on chronic mild stress-induced depression model mice were studied by tail-suspension test, forced swimming test, open field test and sugar-water preference test. Immunohistochemistry was used to detect the effects of magnolol on the expression of BDNF and the incorporation of bromodeoxyuridine (BrdU) into the DNA of hippocampus of depressed mice. Results: Magnolol (40 mg / kg) significantly increased body weight in depression model mice; honokiol (40 mg / kg) significantly increased the number of spontaneous activities of depression model mice in open field; (40mg / kg) significantly reduced the tail suspension and forced swimming time in depression model mice; honokiol (40mg / kg) significantly increased the preference value of depression in model mice. Magnolol can promote hippocampal neuron regeneration, significantly increase the number of BDNF and BrdU positive cells in hippocampus of depression model mice. CONCLUSION: Magnolol (40 mg / kg) has significant antidepressant effect. One of the mechanisms of antidepressant is the promotion of hippocampal neuronal regeneration by increasing the expression of BDNF in hippocampus.