Abstract Title:

Antihepatotoxic benefits of Poria cocos polysaccharides on acetaminophen-lesioned livers in vivo and in vitro.

Abstract Source:

J Cell Biochem. 2019 May ;120(5):7482-7488. Epub 2018 Oct 30. PMID: 30378160

Abstract Author(s):

Ka Wu, Chao Guo, Bin Yang, Xinmou Wu, Weimin Wang

Article Affiliation:

Ka Wu


In our previous study, preliminary data indicates that Poria cocos polysaccharides (PCP) shows beneficial hepatoprotection against acetaminophen (APAP)-induced liver injury in mice. However, biological molecular mechanism warrants to be further discussed. In current study, a number of biochemical tests and immunoassays were subjected to respective PCP-dosed mice in vivo and liver cells in vitro. As a result, PCP-treated mice showed reduced contents of inflammatory cytokines (tumor necrosis factor [TNF]-β and TNFsR-I), enzymological molecules (alanine aminotransferase, aspartate aminotransferase, and lactate dehydrogenase [LDL]), and heat shock protein 90 (Hsp90) after APAP exposure. Additionally, immunostaining assays exhibited that lowered-positive cells of cleaved-caspase-3, cleaved-poly ADP ribose polymerase, and Hsp90-labeled cells in PCP-treated livers were observed, and increased cluster of differentiation 29 (CD29), CD73-positive cells in the spleen were detected. Further, PCP-treated mouse liver cells resulted in increased cell growth, reduced LDL level. Increased proliferating cellnuclear antigen (PCNA), P38 mitogen-activated protein kinase (MAPK)-labeled cells and decreased Hsp90-positive cells in APAP-exposed liver cells were observed dose-dependently after PCP cotreatments. Collectively, our present experimental findings elucidate that PCP beneficially play hepatoprotective effects against APAP-lesioned liver cells in vivo and in vitro, potentially through the molecular mechanisms of suppressing cell death, reducing hepatocellular inflammatory stress and Hsp90 bioactivity.

Study Type : Animal Study, In Vitro Study

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