2, 3, 5, 4-Tetrahydroxystilbene-2-O--d-glucoside prevention of lipopolysaccharide-induced depressive-like behaviors in mice involves neuroinflammation and oxido-nitrosative stress inhibition
2, 3, 5, 4-Tetrahydroxystilbene-2-O--d-glucoside prevention of lipopolysaccharide-induced depressive-like behaviors in mice involves neuroinflammation and oxido-nitrosative stress inhibition
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2,3,5,4-四羟基芪-2-O--d-葡萄糖苷预防脂多糖诱导的小鼠抑郁样行为涉及神经炎症和氧化亚硝化应激抑制
DOI：
10.1097/fbp.0000000000000307
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发表时间：
2017-08-01
影响因子：
1.6
通讯作者：
Ding, Wenbin
中科院分区：
文献类型：
--
作者：
Chen, Zhuo;Huang, Chao;Ding, Wenbin
尽管近年来提出了许多假设，但促进重度抑郁症发展的确切机制在很大程度上是未知的。近年来，针对抑郁症中神经炎症和氧化应激过程的策略受到越来越多的关注。2,3,5,4 -四羟基二苯乙烯-2- o -d-葡萄糖苷（TSG）是一种从中药何首乌中纯化出来的化合物，具有抑制神经炎症和氧化应激的作用。在这种情况下，我们研究了TSG是否影响脂多糖（LPS）诱导的与神经炎症和氧化亚硝化应激相关的抑郁样行为。结果表明，给药0.83mg/kg lps可诱导ICR小鼠在悬尾实验、强迫游泳实验和蔗糖偏好实验中出现典型的抑郁样行为，而TSG（30和60mg/kg）可预防这些行为。进一步分析表明，30和60mg/kg剂量的TSG预处理不仅可以抑制LPS诱导的促炎细胞因子如白细胞介素-1、白细胞介素-6、肿瘤坏死因子-的产生，还可以阻止LPS诱导的小鼠海马和前额叶皮层氧化亚氧化应激的增强。脂多糖诱导的海马和前额叶皮层脑源性神经营养因子水平的下降也被TSG治疗所阻止。总的来说，我们的数据提供了证据，表明TSG可以通过抑制神经炎症和氧化亚硝化应激来应对抑郁样症状。
Although numerous hypotheses have been raised in recent years, the exact mechanisms that promote the development of major depression are largely unknown. Recently, strategies targeting the process of neuroinflammation and oxidative stress in depression have been attracting greater attention. 2, 3, 5, 4-Tetrahydroxystilbene-2-O--d-glucoside (TSG), a compound purified from a traditional Chinese herbal medicine polygonummultiflorum, has been widely reported to inhibit neuroinflammation and oxidative stress. In this context, we investigated whether TSG affects lipopolysaccharide (LPS)-induced depressive-like behaviors in a manner associated with neuroinflammation and oxido-nitrosative stress. Results showed that administration of ICR mice with 0.83mg/kg of LPS-induced typical depressive-like behaviors in the experiments of the tail-suspension test, the forced-swimming test, and sucrose preference, and these behaviors were prevented by TSG treatment (30 and 60mg/kg). Further analysis showed that TSG pretreatment at the doses of 30 and 60mg/kg not only inhibited the production of proinflammatory cytokines induced by LPS, such as interleukin-1, interleukin-6, and tumor necrosis factor-, but also prevented the LPS-induced enhancement of oxido-nitrosative stress in mouse hippocampus and prefrontal cortex. The LPS-induced decreases in brain-derived neurotrophic factor levels in the hippocampus and prefrontal cortex were also prevented by TSG treatment. Generally, our data provide evidence to show that TSG could be used to cope with depressive-like symptoms by inhibition of neuroinflammation and oxido-nitrosative stress.