当前位置： SCI文献检索 > METABOLIC BRAIN DISEASE期刊下所有文献 > Allicin attenuated chronic social defeat stress induced depressive-like behaviors through suppression of NLRP3 inflammasome.

Allicin attenuated chronic social defeat stress induced depressive-like behaviors through suppression of NLRP3 inflammasome.

Abstract：

:Allicin, one of the main biologically active compounds derived from garlic, was previously reported to possess multiple pharmacological activities. Whether allicin protected against chronic social defeat stress (CSDS) induced depressive-like behaviors remained unknown. Thus, our present study for the first time investigated the potential antidepressant effects and the mechanisms of allicin on the CSDS mice model. Thirty minutes before social defeat stress, allicin (2, 10, 50 mg/kg) was treated by intraperitoneal injection. The duration times of CSDS model establishment and allicin intervene were 10 days. Subsequently, the force swimming test (FST), social interaction test (SIT), and sucrose preference test (SPT) were applied for behavioral assessments. The levels of inflammation mediators were determined by commercial ELISA kits. The concentration of iron was tested, and relative protein expressions were measured by western blot. Oxidative stress and apoptosis markers were also detected by commercial kits and western blot. The behavioral defects induced by social defeat stress were obviously improved by allicin. Microglia activation, as well as inflammatory cytokines elevation in the hippocampus of CSDS also down-regulated by administration of allicin. Furthermore, content of iron and protein expressions of key components in iron metabolism were remarkably aberrant changed in the CSDS mice hippocampus, meanwhile, allicin ameliorated this phenomenon. Allicin decreased the production of reactive oxygen species (ROS), malondialdehyde (MDA), and protein carbonyl, and the protein expression of NOX4, as well as up-regulated the activities of superoxide dismutase (SOD) and Nrf2/HO-1 pathway. In addition, allicin attenuated the enhanced neuronal apoptosis. Finally, allicin supplementation inhibited the Nucleotide-binding oligomerization domain containing 3 (NLRP3) inflammasome hyperactivity, and the expressions of inflammasome components, such as ACS, caspase-1, and IL-1β in the hippocampus of CSDS mice. Allicin attenuated depressive-like behaviors of CSDS mice through reducing neuroinflammation, ameliorating iron abnromal accumulation, balacing oxidative stress, and attenuation neuronal apoptosis in the hippocampus via suppression of NLRP3 inflammasome.

journal_name

Metab Brain Dis

journal_title

Metabolic brain disease

authors

Gao W,Wang W,Liu G,Zhang J,Yang J,Deng Z

doi

10.1007/s11011-018-0342-z

subject

Has Abstract

pub_date

2019-02-01 00:00:00

pages

319-329

issue

eissn

0885-7490

issn

1573-7365

pii

10.1007/s11011-018-0342-z

journal_volume

pub_type

杂志文章

在线工具

Allicin attenuated chronic social defeat stress induced depressive-like behaviors through suppression of NLRP3 inflammasome.