Persimmon leaf extract alleviates chronic social defeat stress-induced depressive-like behaviors by preventing dendritic spine loss via inhibition of serotonin reuptake in mice.
Persimmon leaf extract alleviates chronic social defeat stress-induced depressive-like behaviors by preventing dendritic spine loss via inhibition of serotonin reuptake in mice.
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柿叶提取物通过抑制5-羟色胺再摄取来防止小鼠树突棘丢失，从而减轻慢性社会挫败应激诱导的抑郁样行为。
DOI：
10.1186/s13020-022-00609-4
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发表时间：
2022-06-06
期刊：
影响因子：
4.9
通讯作者：
Xu, Jiangping
中科院分区：
文献类型：
--
作者：
Yu, Hui;Shao, Shumin;Xu, Junnan;Guo, Haibiao;Zhong, Zhangfeng;Xu, Jiangping
关键词：
新鲜或干燥的紫苏叶（Diospyros kaki Thunb.）对心脑血管疾病有预防作用。然而，它们的抗抑郁作用和潜在机制尚不清楚。因此，我们研究机制负责Percedium叶提取物（PLE）对慢性社会失败压力（CSDS）诱导的小鼠抑郁样行为的活动。CSDS被用作抑郁症的小鼠模型。我们进行了蔗糖偏好试验（SPT），强迫游泳试验（FST），和悬尾试验（TST），以确定抑郁样行为。棘密度和树突状形态进行了评估，使用高尔基体染色。神经化学物质进行定量微透析，doublecortin免疫荧光，和cAMP使用ELISA试剂盒。最后，通过western blot定量磷酸化cAMP反应元件结合蛋白（CREB）、脑源性神经营养因子（BDNF）、突触后密度突触蛋白-1和蛋白95（PSD 95）的皮质蛋白水平。16 S rRNA基因测序用于检测粪便微生物群。用PLE（30.0-60.0 mg/kg，i.g.）增强蔗糖偏好，减少不动时间在TST和FST，但不影响自发活动。此外，持续的社交失败压力降低了大脑中的树突棘密度和树突长度，以及减少了PSD 95和突触蛋白-1的表达。有趣的是，PLE抑制了树突棘的丢失，增加了突触蛋白的水平。PLE还增加了CSDS小鼠脑中5-HT、cAMP、磷酸化（p）-CREB、BDNF、PSD 95和突触蛋白-1的水平。此外，PLE增加他们的海马齿状回doublecortin阳性细胞计数。CSDS小鼠代表与正常C57 BL/6 J小鼠相比不同的独特粪便微生物群簇，并且该表型被PLE拯救。PLE通过抑制5-羟色胺再摄取和激活cAMP/CREB/BDNF信号通路减轻CSD诱导的抑郁行为和脊髓损伤。同时，PLE影响了CSDS小鼠粪便微生物群的组成。在线版本包含补充材料，可通过10.1186/s13020-022-00609-4获得。
Fresh or dried Persimmon leaves (Diospyros kaki Thunb.) exhibit preventive effects on cardiovascular and cerebrovascular diseases. However, their antidepressant effects and underlying mechanisms are unclear. Thus, we investigated mechanisms responsible for Persimmon leaf extract (PLE) activity on chronic social defeat stress (CSDS)-induced depressive-like behaviors in mice. CSDS was used as a mouse model of depression. We performed the sucrose preference test (SPT), forced swim test (FST), and tail suspension test (TST) to identify depressive-like behavior. Spine density and dendritic morphology were assessed using Golgi staining. Neurochemicals were quantified by microdialysis, doublecortin by immunofluorescence, and cAMP using an ELISA kit. Finally, the levels of cortical proteins of phosphorylated cAMP-response element binding protein (CREB), brain-derived neurotrophic factor (BDNF), postsynaptic density synapsin-1 and protein 95 (PSD95) were quantified by western blot. 16S rRNA gene sequencing was used to detect fecal microbiota. Treatment of CSDS-subjected mice with PLE (30.0–60.0 mg/kg, i.g.) enhanced sucrose preference, decreased immobility times in the TST and FST but did not affect locomotor activity. Furthermore, persistent social defeat stress decreased dendritic spine density and dendritic length in the brain, as well as decreased PSD95 and synapsin-1 expression. PLE, interestingly, inhibited dendritic spine loss and increased synaptic protein levels. PLE also increased brain levels of 5-HT, cAMP, phosphorylated (p)-CREB, BDNF, PSD95, and synapsin-1 in mice subjected to CSDS. Furthermore, PLE increased their doublecortin-positive cell count in the hippocampal dentate gyrus. CSDS mice represented a distinct fecal microbiota cluster which differed compared with normal C57BL/6J mice, and the phenotype was rescued by PLE. PLE alleviated CSDS-induced depressive behaviors and spinal damage by suppressing serotonin reuptake and activating the cAMP/CREB/BDNF signaling pathway. Simultaneously, PLE influenced the composition of the fecal microbiota in CSDS-subjected mice. The online version contains supplementary material available at 10.1186/s13020-022-00609-4.
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