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Rhynchophyllin attenuates neuroinflammation in Tourette syndrome rats via JAK2/STAT3 and NF‐κB pathways
Author(s) -
Hongyan Long,
Mengjiao Zhang,
Chunyan Wang,
Yaruo Huang
Publication year - 2019
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22813
Subject(s) - neuroinflammation , stat3 , western blot , striatum , stat protein , agonist , tumor necrosis factor alpha , endocrinology , chemistry , nf κb , medicine , signal transduction , biology , receptor , inflammation , biochemistry , gene , dopamine
The aim of this study was designed to investigate the effects of rhynchophyllin (RH) on neuroinflammation in Tourette syndrome (TS) rats. TS model was established in rats by the injection of selective 5‐HT2A/2C agonist 1‐(2, 5‐dimethoxy‐4‐iodophenyl)‐2‐aminopropane (DOI). Behavior in DOI‐induced rats was tested. Inflammatory cytokines levels such as interleukin‐1β (IL‐1β), interleukin‐6 (IL‐6), and tumor necrosis factor‐α (TNF‐α) in serum and striatum were detected. The expression levels of janus kinase 2 (JAK2)/signal transducer and transcription activator 3 (STAT3) and nuclear factor (NF)‐κB pathways in striatum were measured by Western blot. Data indicated that RH can significantly reduce the numbers of nodding experiment of TS rats. RH significantly decreased IL‐6, IL‐1β, and TNF‐α in serum and striatum of TS rats, with altered expression of P‐JAK2, P‐STAT3, P‐NF‐κBp65, and P‐IκBα in TS rats, as evidenced by Western blot analysis and immunohistochemistry, suggesting that the regulation of JAK2/STAT3 and NF‐κB pathways might be involved in the mechanism of RH on TS.