肝保护
体内
药理学
乳酸脱氢酶
对乙酰氨基酚
体外
化学
肿瘤坏死因子α
增殖细胞核抗原
分子生物学
生物化学
生物
细胞生长
免疫学
谷胱甘肽
酶
生物技术
作者
Ka Wu,Chao Guo,Bin Yang,Xinmou Wu,Weimin Wang
摘要
Abstract 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 cell nuclear 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.
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