Including infections, drug treatments, and metabolic or geneticĬonsidered as a secondary disease ( 6). Observed in the obstructive subtype ( 3, 4).Ĭholestasis can be caused by pre-existing medical conditions Proliferation, along with centrilobular cholate injury, are Interlobular bile ducts, portal expansion and bile duct Cholestasis is classified asĪnd mechanisms associated with the former type can be broadlyĬlassified as hepatocellular or obstructive. Revealed that the total incidence of cholestasis was 10.26% amongĬhronic liver disease patients ( 2). These results provide an insight into the mechanisms underlying cholestasis development and highlight potential biomarkers for disease diagnosis.Ĭholestasis is characterized by a reduction in bileįlow and bile acid accumulation ( 1), and a higher incidence of thisĬondition is observed in hepatopathy. In addition, principal component analysis demonstrated that the levels of these metabolites differed significantly between the MT and control groups, providing further evidence that they may be responsible for the effects induced by MT.
Metabolomics analysis revealed that this effect was likely to be associated with the regulation of compounds related to MT synthesis and catabolism, and amino acid metabolism, including 5‑aminopentanoate, 5‑methoxytryptamine, L‑tryptophan, threonine, glutathione, L‑methionine, and indolelactate. The histological observations indicated that MT had a protective effect against ANIT‑induced hepatic tissue damage. The results revealed that the serum levels of alanine aminotransferase, aspartate aminotransferase, total bilirubin, direct bilirubin, γ‑glutamyl transpeptidase, and alkaline phosphatase were reduced in rats with ANIT‑induced cholestasis that were treated with MT. Active components in the serum were identified by gas chromatography‑mass spectrometry, while biomarkers and biochemical pathways were identified by multivariate data analysis. Serum biochemical parameters were measured and liver tissue samples were subjected to histological analysis. Rats were administered ANIT by intraperitoneal injection and then sacrificed 36 h later. The present study investigated the anti‑cholestatic effect of melatonin (MT) against α‑naphthyl isothiocyanate (ANIT)‑induced liver injury in rats and screened for potential biomarkers of cholestasis.
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