Biotechnology and Bioprocess Engineering 2022; 27(3): 336-343  
Hepatic Protective Effects of Jujuboside B through the Modulation of Inflammatory Pathways
In-Chul Lee and Jong-Sup Bae
In-Chul Lee
Department of Cosmetic Science and Technology, Seowon University, Cheongju 28674, Korea
Jong-Sup Bae*
College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook National University, Daegu 41566, Korea
Tel: +82-53-950-8570; Fax: +82-53-950-8557
E-mail: baejs@knu.ac.kr
Received: February 13, 2022; Revised: February 21, 2022; Accepted: February 21, 2022; Published online: June 30, 2022.
© The Korean Society for Biotechnology and Bioengineering. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
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 enzymelinked 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.
Keywords: jujubisode B, liver failure, inflammation, toll-like receptor, lipopolysaccharide


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