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Published:
May 28, 2022DOI:
10.4314/tjpr.v21i3.9Keywords:
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Main Article Content
Buddleoside inhibits TLR4-related pathway in a mouse model of acute liver failure, promotes autophagy, and inhibits inflammation
Abstract
Purpose: To study the inhibitory influence of buddleoside on TLR4-associated pathway, autophagy and inflammation in a mouse model of acute liver failure (ALF).
Methods: Sixty male C57BL/6 mice were assigned to 5 groups: control, model, and three dose-groups of buddleoside, with 12 mice per group. Levels of interleukin (IL)-1, IL-6, TLR4 pathway-associated proteins, and autophagy-related proteins in each group were determined; cell adhesion in each group was also analyzed.
Results: Levels of TLR4, MAPK and NF-кB-related pathways in model mice were significantly upregulated, relative to control mice, but they were more down-regulated in the 3 anthocyanin groups than in model group (p < 0.05). There were significantly higher levels of TNF-α, IL- and IL-6 in model mice than in the control group, but they were down-regulated in high-, medium- and low-dose mice, relative to model mice. The population of adherent cells was significantly higher in ALF mice than in controls, but
there were markedly lower numbers of these cells in the 3 anthocyanin-treated mice than in model mice (p < 0.05).
Conclusion: Buddleoside mitigates ALF in mice by down-regulating inflammatory factors, reducing serum levels of ALT and AST, and up-regulating autophagy-related protein expressions by activating TLR4/MAPK/NF-кB signaling pathway. Thus, buddleoside may be useful in the treatment of acute liver failure, but this has to be curtained through clinical trials.
