黄精多糖对急性抑郁小鼠模型的改善作用及机制

目的:探索黄精多糖对急性抑郁模型小鼠的改善作用及机制。方法:将60只ICR小鼠分为正常组、帕罗西汀对照组（10 mg/kg）、黄精多糖低剂量组（100 mg/kg）、黄精多糖中剂量组（200 mg/kg）和黄精多糖高剂量组（400 mg/kg）。预防给予黄精多糖3周后，通过体重监测和空场实验表现，研究黄精多糖对小鼠体重和自主活动的影响；通过悬尾实验和强迫游泳实验，研究黄精多糖对急性抑郁模型小鼠的行为影响；通过分析皮层中5-羟色胺（5-hydroxytryptamine，5-HT）、去甲肾上腺素（norepinephrine，NE）和多巴胺（dopamine，DA），血清中肿瘤坏死因子-α（tumor necrosis factor，TNF-α）和白介素-10（interleukin-10，IL-10），海马中色氨酸（Tryptophan，TRP）及其代谢产物5-羟吲哚乙酸（5- hydroxyindolacetic acid，5-HIAA）和3-羟基犬尿氨酸（3-hydroxycaninuric acid，3-HK）等生化指标，探究黄精多糖抗抑郁作用的分子机制。结果:黄精多糖显著缩短了行为绝望模型小鼠在悬尾和强迫小鼠游泳实验中的不动时间（P<0.05）；在空场实验中，各组小鼠运动路程和运动时间等自主活动度无显著性差异（P>0.05）。与空白组相比，黄精多糖组（200和400 mg/kg）小鼠脑组织5-HT、DA和NE水平显著升高（P<0.05），血清中TNF-α和IL-10活性降低（P<0.05），海马中TRP和3-HK水平下调（P<0.05）。结论:黄精多糖（200和400 mg/kg）可通过上调急性绝望抑郁模型动物脑内的单胺类神经递质、抑制神经炎性反应和调节色氨酸代谢通路起到改善抑郁的作用。

Protective Effects and Mechanism of Polysaccharide from Polygonati rhizoma on Behavioral Despair Mice

Objective: To study the protective effects of polysaccharide from Polygonati rhizoma (PSP) on acute behavioral despair mice and the underlying mechanisms. Methods: A total of 60 ICR mice were randomly divided into the control group, the paroxetine group (10 mg/kg), PSP-low group (100 mg/kg), PSP-medium group (200 mg/kg), and PSP-high group (400 mg/kg). After 3 weeks of administration, the effect of PSP on the body weight and locomotor activity of mice was investigated by body weight and open field. The tail suspension and the forced swimming test were conducted to evaluate the antidepressant effect of PSP. In addition, 5-hydroxytryptamine (5-HT), norepinephrine (NE), dopamine (DA) levels in cortex, tumor necrosis factor (TNF-α), interleukin-10 (IL-10) levels in serum as well as tryptophan (TRP), 5-hydroxyindolacetic acid (5-HIAA) and 3-hydroxycaninuric acid (3-HK) contents in hippocampus of mice were evaluated to explore the molecular mechanism of antidepressant effect. Results: The PSP administration remarkably shortened the immobility time of the behavioral despair model mice both in tail suspension test and forced swimming test (P<0.05), showing the antidepressant activity. At the same time, PSP had no influence on the body weight and locomotor activity of mice (P>0.05). Moreover, PSP (200 and 400 mg/kg) significantly elevated the levels of 5-HT, DA and NE in cortex (P<0.05), decreased the TNF-α and IL-10 release in serum (P<0.05), as well as inhibited the levels of TRP and 3-HK (P<0.05) in hippocampus of mice compared to those of control group. Conclusion: PSP (200 and 400 mg/kg) exerted remarkable antidepressant activity in behavioral despair mice probably by promoting monoamine neurotransmitter release, inhibiting inflammatory cytokines levels, and regulating tryptophan metabolism.