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논문 기본 정보

자료유형
학술저널
저자정보
Xiang Xu (Yanbian University) Lan Jin (Yanbian University) Tong Jiang (Yanbian University) Ying Lu (Yanbian University) Fumie Aosai (Shinshu University) Hu-Nan Piao (Affliated Hospital of Yanbian University) Guang-Hua Xu (Yanbian University) Cheng-Hua Jin (Yanbian University) Xue-Jun Jin (Yanbian University) Juan Ma (Yanbian University) Lian-Xun Piao (Yanbian University)
저널정보
고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.44 No.5
발행연도
2020.9
수록면
704 - 716 (13page)

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초록· 키워드

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Background: Ginsenoside Rh2 (GRh2) is a characterized component in red ginseng widely used in Korea and 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 not been clarified yet.
Methods: The effect of GRh2 against T. gondii was assessed under in vitro and in vivo experiments. The BV2 cells were infected with tachyzoites of T. gondii RH strain, and the effects of GRh2 were evaluated by MTT 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/c mice inoculated with lethal amounts of tachyzoites with or without GRh2 treatment.
Results and conclusion: The GRh2 treatment significantly inhibited the proliferation of T. gondii under in vitro and in vivo studies. Furthermore, GRh2 blocked the activation of microglia and specifically decreased the release of inflammatory mediators in response to T. gondii infection through TLR4/NF-kB signaling pathway. In mice, GRh2 conferred modest protection from a lethal dose of T. gondii. After the treatment, 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 findings indicate 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 to treat toxoplasmic encephalitis.

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ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References

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UCI(KEPA) : I410-ECN-0101-2020-524-001313007