Echinocystic acid reduces reserpine-induced pain/depression dyad in mice

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• 作者：Shuo Li ; Jing Han ; Dong-sheng Wang ; Bin Feng ; Ya-ting Deng…
• 关键词：Echinocystic acid ; Pain ; Depression ; NMDA receptor ; Serotonin ; Hippocampus
• 刊名：Metabolic Brain Disease
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：31
• 期：2
• 页码：455-463
• 全文大小：1,093 KB
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• 作者单位：Shuo Li (1)
  Jing Han (1)
  Dong-sheng Wang (2)
  Bin Feng (1)
  Ya-ting Deng (1)
  Xin-shang Wang (1)
  Qi Yang (1)
  Ming-gao Zhao (1)
  
  1. Department of Pharmacology, School of Pharmacy, The Fourth Military Medical University, Xi’an, 710032, China
  2. Department of Orthopedics, Jinling Hospital, Clinical School of Nanjing, Second Military Medical University, Nanjing, 210002, China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Neurology
  Biochemistry
  Oncology
  
• 出版者：Springer Netherlands
• ISSN：1573-7365

文摘

Chronic pain has consistently been correlated with depression. Echinocystic acid (EA), a natural triterpone enriched in various herbs and used for medicinal purpose in many Asian countries, exhibits anti-inflammatory and analgesic activities. However, little is known the effects of EA on the depression. In present study, we investigated the anti-depression activities in the mouse model of reserpine-induced pain-depression dyad. Reserpine (1 mg/kg subcutaneously daily for 3 days) caused significant depression-like behaviors and pain sensation. Subsequent treatment of EA (5 mg/kg intragastrically daily for 5 days) attenuated the reserpine-induced pain/depression dyad as shown by the increase of pain threshold and the behaviors in forced swimming test, tail suspension test, and open field test. Furthermore, treatment of EA reversed the decrease of biogenic amines (norepinephrine, dopamine, and serotonin) in the brain region of hippocampus, a structure involved in the formation of emotional disorders. Levels of serotonin receptor 5-HT1A were decreased and levels of 5-HT2A were increased in the reserpine-injected mice. Treatment of EA could restore the alterations of serotonin receptors. At the same time, the increase in GluN2B-containing NMDA receptors, p-GluA1-Ser831, PSD-95 and CaMKII were integrated with the increase in caspase-3 and iNOS levels in the hippocampus of the reserpine-injected mice. EA significantly reversed the changes of above proteins. However, EA did not affect the levels of GluN2A-containing NMDA receptors and the total levels of GluA1 and p-GluA1-Ser845. Our study provides strong evidence that EA attenuates reserpine-induced pain/depression dyad partially through regulating the biogenic amines levels and GluN2B receptors in the hippocampus.