Journal of biochemical and molecular toxicology · 2019
Gastrodin attenuates neuroinflammation in DOI-induce Tourette syndrome in rats.
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Long Hongyan, Wang Chunyan, Ruan Jie, Zhang Mengjiao, Huang Yaruo
Аннотация
OBJECTIVE: Tourette syndrome (TS) is a chronic neuropsychiatric disorder. Its clinical manifestations are involuntary and recurrent muscle twitch, resulting in motor twitch and occurrence twitch. Traditional Chinese medicine has obvious advantages in treating TS. The aim of this study was to investigate the effects and mechanism of gastrodin on 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI)-induced TS in rats.
METHODS: TS model was induced by DOI. Behaviors in TS rats were detected. The striatum, serum inflammatory factors interleukin-6, interleukin-1β, and tumor necrosis factor-a were detected by enzyme-linked immunosorbent assay. Western blot technique was used to detect the expressions of TLR/NF-κB and TLR/MAPK signaling pathways in the striatum.
RESULTS: Gastrodin can significantly improve behavioral changes of TS rats induced by DOI, reduce inflammatory factors in serum and striatum in TS rats, and inhibit activation of TLR/NF-κB and TLR/MAPK signaling in striatum in TS rats.
CONCLUSION: Gastrodin can significantly relieve the TS induced by DOI in rats. Its mechanism is related to the inhibition of striatal TLR/NF-κB and TLR/MAPK signaling activation.
METHODS: TS model was induced by DOI. Behaviors in TS rats were detected. The striatum, serum inflammatory factors interleukin-6, interleukin-1β, and tumor necrosis factor-a were detected by enzyme-linked immunosorbent assay. Western blot technique was used to detect the expressions of TLR/NF-κB and TLR/MAPK signaling pathways in the striatum.
RESULTS: Gastrodin can significantly improve behavioral changes of TS rats induced by DOI, reduce inflammatory factors in serum and striatum in TS rats, and inhibit activation of TLR/NF-κB and TLR/MAPK signaling in striatum in TS rats.
CONCLUSION: Gastrodin can significantly relieve the TS induced by DOI in rats. Its mechanism is related to the inhibition of striatal TLR/NF-κB and TLR/MAPK signaling activation.