Abstract
Objective The aim of this study was to evaluate the effects of a modified Xiaohua Funing decoction (Xfd) on acute liver failure (ALF) and determine whether the protective mechanisms are related to alterations in the gut microbiota. Methods An animal model of ALF was induced by intraperitoneal injection of D-galactosamine (D-Gal, 0.5 g/kg) and lipopolysaccharide (LPS, 100 μg/kg). Male BALB/c mice were randomly divided into the following 4 groups: the control group (saline, Con), model group (D-Gal/LPS, Mod), silymarin pretreatment group (200 mg/kg, Sil), and modified Xfd pretreatment group (650 mg/kg, Xfd). The Sil and Xfd groups received the respective intervention orally for 14 days and 2 h before D-Gal/LPS treatment. The liver injury markers included alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels and liver histology. 16S rRNA gene sequencing was performed to assess the effects on the caecum content. Results D-Gal/LPS treatment caused severe ALF, illustrating that the ALF model was successfully established. The administration of Sil and Xfd greatly reduced the serum ALT and AST levels and improved the pathological signs of liver injury. However, no significant difference was found between the two groups. In contrast to the Mod group, the Sil and Xfd groups showed a shift toward the Con group in terms of the gut microbiota structure. The abundances of Firmicutes and Bacteroidetes and the Bacteroidetes/Firmicutes ratio in the Mod group significantly differed from those in the Con group. The Sil and Xfd groups showed restoration of the disordered microbiota. Significantly increased relative abundances of Lachnospiraceae_NK4A136_group and Candidatus_Saccharimonas and a markedly decreased Muribaculaceae abundance were found in the Sil and Xfd mice compared with those in the Mod mice (P < 0.01, P < 0.05). Interestingly, a negative correlation was observed between the abundances of the gut microbiota constituents, specifically Clostridia_UCG-014, and ALT and AST levels. Conclusion In summary, our results indicate that Xfd may protect the liver and modify the gut microbiota in ALF mice.
Highlights
Acute liver failure (ALF) caused by extensive hepatocyte necrosis is a fatal clinical syndrome and has been well characterized
Mouse Body Weight. ere was a gradual increase in body weight in all groups
Compared with the model group (Mod) group, the silymarin group (Sil) and Xiaohua Funing decoction (Xfd) groups showed remarkably reduced ALT and AST levels, and the Xfd mice showed no significant decreases in ALT and AST levels compared with those in the Sil mice (Figure 4)
Summary
Acute liver failure (ALF) caused by extensive hepatocyte necrosis is a fatal clinical syndrome and has been well characterized. The underlying mechanisms are not fully understood [1]. Studies have demonstrated that alterations in the gut microbiota play a crucial role in the pathogenesis of liver diseases [2, 3]. During the early stage of ALF, the systemic and intestinal immune systems are suppressed, which leads to a rapid loss of normal liver function, multiple organ failure, and even death [4]. Despite advances in medical therapies, effective clinical ALF treatment is lacking [5, 6]. In China, Chinese herbal medicine (CHM) therapy for ALF has been widely used.
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