Abstract
Yin-Chen-Hao-Tang (YCHT) is a famous Chinese medicine formula which has long been used in clinical practice for treating various liver diseases, such as liver fibrosis. However, to date, the mechanism for its anti-fibrotic effects remains unclear. In this paper, an ultra-performance liquid chromatography-time-of-flight mass spectrometry (UPLC-TOF-MS)-based metabolomic study was performed to characterize dimethylnitrosamine (DMN)-induced liver fibrosis in rats and evaluate the therapeutic effects of YCHT. Partial least squares-discriminant analysis (PLS-DA) showed that the model group was well separated from the control group, whereas the YCHT-treated group exhibited a tendency to restore to the controls. Seven significantly changed fibrosis-related metabolites, including unsaturated fatty acids and lysophosphatidylcholines (Lyso-PCs), were identified. Moreover, statistical analysis demonstrated that YCHT treatment could reverse the levels of most metabolites close to the normal levels. These results, along with histological and biochemical examinations, indicate that YCHT has anti-fibrotic effects, which may be due to the suppression of oxidative stress and resulting lipid peroxidation involved in hepatic fibrogenesis. This study offers new opportunities to improve our understanding of liver fibrosis and the anti-fibrotic mechanisms of YCHT.
Highlights
Liver fibrosis is a prevalent chronic liver disease characterized by the increased hepatic deposition of extracellular matrix proteins [1]
The serum levels of fatty acids were significantly lower in the fibrotic model rats than in the controls, while the levels of Lyso-PCs exhibited various changes between the two groups (Figure 5). These results suggest that an impaired lipid metabolism may play a crucial role in the pathogenesis of liver fibrosis
A clear separation of the model and control groups was achieved, and the YCHT group exhibited a tendency to restore to the controls
Summary
Liver fibrosis is a prevalent chronic liver disease characterized by the increased hepatic deposition of extracellular matrix proteins [1]. Numerous works have centered on gene expression, protein function, as well as conventional pathophysiological studies on the liver fibrosis [4,5]. The mechanisms for liver fibrosis have been dramatically elucidated but are still not fully understood. As such a complex and multifactorial process, liver fibrosis involves expressed genes and proteins, and the changes of endogenous metabolites, and to investigate the metabolic variations might be expected to provide new insights into the pathogenesis of fibrotic process [6]
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