Abstract
Total glucosides of paeony (TGP) have been confirmed to be hepatoprotective. However, the underlying mechanism is largely unclear. In this study, we investigated the metabolic profiles of urine and serum in rats with carbon tetrachloride- (CCl4-) induced experimental liver injury and TGP administration by using ultra-performance liquid chromatography-mass spectrometry (UPLC-MS). The vehicle or a single dose of TGP was intragastrically administered to Wistar rats once a day for 14 consecutive days. To induce ALI, 50% CCl4 was injected intraperitoneally into these rats 2 hours after the last time administration of saline of TGP at the 14th day. The results indicated that TGP administration could protect rats from CCl4-induced ALI and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) elevation, as well as hepatocyte apoptosis and inflammation. Furthermore, metabolomics analysis showed that TGP treatment significantly attenuated CCl4-triggered deregulation of multiple metabolites in both urine and serum, including glycine, alanine, proline, and glutamine. Metabolite set enrichment and pathway analyses demonstrated that amino acid cycling and glutathione metabolism were two main pathways involved in CCl4-induced experimental liver injury and TGP administration. Taken together, these findings revealed that regulation of metabolites potentially plays a pivotal role in the protective effect of TGP on ALI.
Highlights
Sudden hepatocyte damage induced by drugs, hepatitis virus infections, hepatic ischemia reperfusion, and toxins often causes ALI, which represents a common pathological basis of various liver diseases [1, 2]
Metabolite set enrichment and pathway analyses demonstrated that amino acid cycling and glutathione metabolism were two main pathways involved in carbon tetrachloride- (CCl4-)induced experimental liver injury and Total glucosides of paeony (TGP) administration
To determine the efficacy of TGP extract (Paeoniflorin: 42.64%, Albiflorin: 15.20%, as shown in Figures 1(a) and 1(b)) on CCl4-induced ALI, the left lobes of liver tissue were collected from groups 1–3 and subjected to hematoxylin and eosin (H&E) staining
Summary
Sudden hepatocyte damage induced by drugs, hepatitis virus infections, hepatic ischemia reperfusion, and toxins often causes ALI, which represents a common pathological basis of various liver diseases [1, 2]. Long-term liver injury often leads to liver fibrosis and hepatocellular carcinoma, which are life-threatening conditions associated with high morbidity and mortality [3]. The prevention of ALI occurrence and progression is essential for clinical treatment of liver diseases. Appropriate balance between cell death and compensatory cell proliferation is critical for normal physiological functions of liver. Imbalance of hepatocyte death and compensatory proliferation plays a pivotal role in the outcome of ALI. The underlying mechanisms are still only poorly understood
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