Hepatic Protective Effects of Jujuboside B through the Modulation of Inflammatory Pathways

Jujubisode B (JB) is a product extracted from the seeds of Zizyphi Spinosi Semen with the pharmacological activities such as antianxiety, anti-inflammation, and antiplatelet aggregation. In this study, we evaluated the effect of JB on liver failure induced by lipopolysaccharide (LPS) and the underly...

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Published inBiotechnology and bioprocess engineering Vol. 27; no. 3; pp. 336 - 343
Main Authors Lee, In-Chul, Bae, Jong-Sup
Format Journal Article
LanguageEnglish
Published Seoul The Korean Society for Biotechnology and Bioengineering 01.06.2022
Springer Nature B.V
한국생물공학회
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Summary:Jujubisode B (JB) is a product extracted from the seeds of Zizyphi Spinosi Semen with the pharmacological activities such as antianxiety, anti-inflammation, and antiplatelet aggregation. In this study, we evaluated the effect of JB on liver failure induced by lipopolysaccharide (LPS) and the underlying mechanisms. We established a hepatic injury model by LPS administration. Methyl Thiazolyl Tetrazolium (MTT) assay was used to detect the cellular viability effect of JB on cell proliferation. Alanine aminotransferase (ALT), aspartate aminotransferase (AST) levels, and histological analysis were used to evaluate the hepatic protective effect of JB. Western blot or enzyme-linked immunosorbent assay (ELISA) was used to detect protein expression. JB suppressed LPS-induced mice lethality and serum levels of liver damage markers without affecting the survival rate. Additionally, JB reduced inflammatory cytokines and toll-like receptor 4 (TLR4) protein expression, which were increased by LPS. LPS induced hepatic injury was also suppressed by JB treatment. The mechanism of this hepatoprotective effect of JB is mediated by the inhibiting the increased MyD88-dependent signaling, mitogen-activated protein kinase activation, and expression of inflammatory genes hepatic failure by LPS. These results suggest that JB is a potential therapeutic agent for liver disease through the inhibition of the TLR4 signaling pathway.
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ISSN:1226-8372
1976-3816
DOI:10.1007/s12257-022-0049-1