Chen Jiang, Zhou Tian, Guo A-Min, Chen Wen-Bing, Lin Dong, Liu Zi-Yang, Fei Er-Kang
Laboratory of Synaptic Development and Plasticity, Institute of Life Science, Nanchang University, Nanchang 330031, China.
Department of Biological Science, School of Life Sciences, Nanchang University, Nanchang 330031, China.
Biology (Basel). 2020 Oct 26;9(11):359. doi: 10.3390/biology9110359.
Metformin, a first-line drug for type 2 diabetes mellitus (T2DM), has been found to reduce depressive symptoms in patients with comorbid depression and other diseases. However, it is largely unclear how metformin ameliorates depressive-like behaviors. Here, we used lipopolysaccharide (LPS) to induce depressive-like behaviors in mice and found that LPS-treated mice exhibited increased immobility in the forced swimming test (FST) and tail suspension test (TST), as well as increased glutamatergic transmission. Furthermore, metformin administration in the LPS-treated mice ameliorated depressive-like behaviors and elevated glutamatergic transmission. Our results suggest that metformin has antidepressant effects and can correct abnormal glutamatergic transmission, providing an insight into the underlying mechanism by which metformin acts against depression.
二甲双胍是2型糖尿病（T2DM）的一线治疗药物，已被发现可减轻合并抑郁症及其他疾病患者的抑郁症状。然而，二甲双胍改善抑郁样行为的具体机制尚不清楚。在此，我们使用脂多糖（LPS）诱导小鼠出现抑郁样行为，发现LPS处理的小鼠在强迫游泳试验（FST）和悬尾试验（TST）中静止不动的时间增加，同时谷氨酸能传递增强。此外，给LPS处理的小鼠施用二甲双胍可改善抑郁样行为，并提高谷氨酸能传递。我们的结果表明，二甲双胍具有抗抑郁作用，可纠正异常的谷氨酸能传递，为二甲双胍抗抑郁的潜在机制提供了见解。
