Details

Autor(en) / Beteiligte

• Xiang Xu
• Lan Jin
• Tong Jiang
• Ying Lu
• Fumie Aosai
• Hu-Nan Piao
• Guang-Hua Xu
• Cheng-Hua Jin
• Xue-Jun Jin
• Juan Ma
• Lian-Xun Piao

Titel

Ginsenoside Rh2 attenuates microglial activation against toxoplasmic encephalitis via TLR4/NF- B signaling pathway

Ist Teil von

• Journal of Ginseng Research, 2020, 44(5), , pp.704-716

Ort / Verlag

고려인삼학회

Erscheinungsjahr

2020

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• Background: Ginsenoside Rh2 (GRh2) is a characterized component in red ginseng widely used in Koreaand China. GRh2 exhibits a wide range of pharmacological activities, such as anti-inflammatory, antioxidant,and anticancer properties. However, its effects on Toxoplasma gondii (T. gondii) infection have notbeen clarified yet. Methods: The effect of GRh2 against T. gondii was assessed under in vitro and in vivo experiments. TheBV2 cells were infected with tachyzoites of T. gondii RH strain, and the effects of GRh2 were evaluated byMTT assay, morphological observations, immunofluorescence staining, a trypan blue exclusion assay,reverse transcription PCR, and Western blot analyses. The in vivo experiment was conducted with BALB/cmice inoculated with lethal amounts of tachyzoites with or without GRh2 treatment. Results and conclusion: The GRh2 treatment significantly inhibited the proliferation of T. gondii underin vitro and in vivo studies. Furthermore, GRh2 blocked the activation of microglia and specificallydecreased the release of inflammatory mediators in response to T. gondii infection through TLR4/NF-kBsignaling pathway. In mice, GRh2 conferred modest protection from a lethal dose of T. gondii. After thetreatment, the proliferation of tachyzoites in the peritoneal cavity of infected mice markedly decreased. Moreover, GRh2 also significantly decreased the T. gondii burden in mouse brain tissues. These findingsindicate that GRh2 exhibits an antieT. gondii effect and inhibits the microglial activation through TLR4/NF-kB signaling pathway, providing the basic pharmacological basis for the development of new drugs totreat toxoplasmic encephalitis. KCI Citation Count: 23