Senegenin exerts anti-depression effect in mice induced by chronic un-predictable mild stress via inhibition of NF-κB regulating NLRP3 signal pathway |
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| Institution: | 1. Clinical Medical College, Chengdu University of TCM, Chengdu 610075, China;2. Department of Ophthalmology, Chengdu University of TCM, Chengdu 610075, China;3. General Clinical Research Center, First Affiliated Hospital of Nanjing Medical University, Nanjing, China;4. Department of Pharmacy, First Affiliated Hospital of Nanjing Medical University, Nanjing, China;5. Department of Traditional Chinese Medicine, The Third People''s Hospital of Chengdu, 82 Qing Long Street, Chengdu 610031, China;6. Neurobiology Laboratory, Jiangsu Center for Drug Screening, China Pharmaceutical University, Jiangsu, Nanjing 210009, China;7. University College London, United Kingdom;1. Department of Anesthesiology, Zhongda Hospital, Medical School, Southeast University, Nanjing, China;2. Department of Anesthesiology, Jiangsu Cancer Hospital, Jiangsu Cancer Institute, Affiliated Hospital of Nanjing Medical University, Nanjing, China;3. Department of Anesthesiology, Obstetrics and Gynecology Hospital Affiliated to Nanjing Medical University, Nanjing, China;1. Department of Physiology, School of Pharmaceutical Sciences, Nanjing Tech University, Nanjing 210009, PR China;2. Department of Pharmaceutical, Nanjing First Hospital, China Pharmaceutical University, Nanjing 210000, PR China |
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| Abstract: | Depressive disorder is a kind of affective disturbance disease. Emerging evidence has suggested that inflammation may contribute to the pathologic process of depressive disorder. Senegenin (SEN), a major bioactive constituent in Polygala tenuifolia Willd, has much bioactivity including anti-inflammatory and neuroprotection effects. However, the mechanism of its anti-depressant effect in mice remains unknown. This study aimed to explore the anti-depressant effects of SEN on behavioral changes and inflammatory responses in mice induced by chronic un-predictable mild stress (CUMS). SEN treatment remarkably ameliorated CUMS-induced behavioral abnormalities, such as improving locomotor activity, decreasing immobility time in Tail suspension test (TST) and Forced swimming test (FST), and increasing sucrose intake in Sucrose preference test (SPT). Additionally, SEN improve protein levels of Brain-derived neurotrophic factor (BDNF) and Neurotrophin-3 (NT-3) expression.In response to stress, p65 was activated to promote production of pro-IL-1β, and then cleaved to mature IL-1β by NOD-like receptor protein 3 (NLRP3) inflammasome pathway in hippocampus of CUMS mice. After SEN treatment, protein activation related to NLRP3 inflammasome pathway was down-regulated, which inhibited IL-1β secretion. These results demonstrate that SEN plays an important role in treatment CUMS-induced depression in mice, possibly via suppression of pathway activation associated with NLRP3 inflammasome. |
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