4.4 Article

Protective Effect of Schisandra chinensis Polysaccharides Against the Immunological Liver Injury in Mice Based on Nrf2/ARE and TLR4/NF-κB Signaling Pathway

期刊

JOURNAL OF MEDICINAL FOOD
卷 22, 期 9, 页码 885-895

出版社

MARY ANN LIEBERT, INC
DOI: 10.1089/jmf.2018.4377

关键词

anti-inflammatory; antioxidant; concanavalin A; hepatoprotection

资金

  1. Natural Science Foundation of Jilin Province [20170309006YY, 20170307016YY]
  2. Science and Technology Project of Jilin Provincial Education Department [JJKH20180373KJ]

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We have previously demonstrated the hepatoprotective effect of Schisandra chinensis polysaccharides (SCP) against the liver injury induced by alcohol, high-fat diet, and carbon tetrachloride in mice. In this study, we investigated the effect of SCP against the immunological liver injury induced by concanavalin A (Con A) in mice. The results showed that SCP could significantly reduce the level of alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), interleukin-1 beta (IL-1 beta), and interleukin-6 (IL-6) in the serum of mice with immunological liver injury. SCP could significantly decrease the content of malondialdehyde (MDA) and nitric oxide (NO) and increase the activity of superoxide dismutase (SOD) and glutathione (GSH) in the liver tissue. SCP could significantly increase the number of CD4(+) and decrease the number of CD8(+) in the peripheral blood, and elevate the ratio of CD4(+)/CD8(+). SCP could significantly downregulate the expression of Kelch-like ECH-associated protein 1 (Keap1) and upregulate the expression of nuclear factor-erythroid 2-related factor2 (Nrf2) and downstream gene heme oxygenase-1 (HO-1), and downregulate the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MyD88), and nuclear factor-kappa B (NF-kappa B) proteins. This study indicates that SCP can reduce the release of a large number of inflammatory factors to inhibit the oxidative stress in mice with the immunological liver injury induced by Con A, and its mechanism is closely related to the regulation of Nrf2/antioxidant response element and TLR4/NF-kappa B signaling pathways.

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