In vivo and in vitro studies using Clonorchis sinensis adult-derived total protein (CsTP) on cellular function and inflammatory effect in mouse and cell model

Clonorchis sinensis ( C. sinensis ) can induce a food-borne parasitic disease (clonorchiasis). Numerous studies have analyzed functional proteins, immunologic factors, pro-inflammatory cytokines, and cell signaling transduction that promote the development of clonorchiasis. In a previous study, it w...

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Veröffentlicht in:Parasitology research (1987) 2020-05, Vol.119 (5), p.1641-1652
Hauptverfasser: Shang, Mei, Sun, Hengchang, Wu, Yinjuan, Gong, Yu, Tang, Zeli, Meng, Fangang, He, Lei, Yu, Xinbing, Huang, Yan, Li, Xuerong
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Sprache:eng
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Zusammenfassung:Clonorchis sinensis ( C. sinensis ) can induce a food-borne parasitic disease (clonorchiasis). Numerous studies have analyzed functional proteins, immunologic factors, pro-inflammatory cytokines, and cell signaling transduction that promote the development of clonorchiasis. In a previous study, it was shown that C. sinensis adult-derived total protein ( Cs TP) might be involved in the pathogenesis and development of liver fibrosis via bringing about Th2 immune response. In the present study, further investigation of Cs TP on cellular function and inflammatory effect in vitro and in vivo has been elicited. Cs TP induced inflammation and autophagy as evidenced by upregulation of TNF-α, IFN-γ, and autophagic markers LC3B and P62. Exposed to Cs TP upregulated the antiapoptotic gene Bcl-2 expression, diminished the apoptosis induced by H 2 O 2 , but promoted the proliferation and migration of LX-2 cells in proper concentration range. Additionally, the protein levels of p-AKT and p-mTOR were repressed in response to Cs TP, suggesting a correlation of blocking the activation of mTOR/AKT signaling pathway. These results revealed that Cs TP might exacerbate hepatic pathological changes by regulating cell proliferation, apoptosis, autophagy, and inflammation in the liver and LX-2 cells. Some effects might be partially involved in the mTOR and AKT pathways.
ISSN:0932-0113
1432-1955
DOI:10.1007/s00436-020-06651-1