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Details

Autor(en) / Beteiligte
Titel
Arctigenin ameliorates depression-like behaviors in Toxoplasma gondii-infected intermediate hosts via the TLR4/NF-κB and TNFR1/NF-κB signaling pathways
Ist Teil von
  • International immunopharmacology, 2020-05, Vol.82, p.106302-106302, Article 106302
Ort / Verlag
Netherlands: Elsevier B.V
Erscheinungsjahr
2020
Quelle
Access via ScienceDirect (Elsevier)
Beschreibungen/Notizen
  • [Display omitted] •Arctigenin ameliorates T. gondii infection-induced depressive behaviors in mice.•Arctigenin attenuates excessive microglial activation and neuroinflammation.•Arctigenin suppresses both TLR4/NF-κB and TNFR1/NF-κB signaling pathways.•Arctigenin decreases the T. gondii burden in BV2 cells and brain tissues. Toxoplasma gondii (T. gondii) is a known neurotropic protozoan that remains in the central nervous system and induces neuropsychiatric diseases in intermediate hosts. Arctigenin (AG) is one of the major bioactive lignans of the fruit Arctium lappa L. and has a broad spectrum of pharmacological activities such as neuroprotective, anti-inflammatory and anti-T. gondii effects. However, the effect of AG against depressive behaviors observed in T. gondii-infected hosts has not yet been clarified. In the present study, we analyzed the effects of AG against T. gondii-induced depressive behaviors in intermediate hosts using a microglia cell line (BV2 cells) and brain tissues of BALB/c mice during the acute phase of infection with the RH strain of T. gondii. AG attenuated microglial activation and neuroinflammation via the Toll-like receptor/nuclear factor-kappa B (NF-κB) and tumor necrosis factor receptor 1/NF-κB signaling pathways, followed by up-regulating the dopamine and 5-hydroxytryptamine levels and inhibiting the depression-like behaviors of hosts. AG also significantly decreased the T. gondii burden in mouse brain tissues. In conclusion, we elucidated the effects and underlying molecular mechanisms of AG against depressive behaviors induced by T. gondii infection.

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