AI Article Synopsis
- The study investigates whether serum autotaxin (ATX) activity is a potential target for regulating liver fibrosis and examines the protective and antifibrotic effects of histidine in a rat model.
- Rats were divided into five groups: one control and others treated with varying combinations of thioacetamide (TAA) and histidine to assess liver health indicators.
- Results showed that TAA increased liver damage markers, while histidine treatment significantly reduced these markers and improved antioxidant capacity, suggesting histidine's role in protecting against liver fibrosis.
Article Abstract
The aim of this study was to explain whether serum autotaxin (ATX) activity might be a target for regulation of liver fibrosis and to evaluate the hepatoprotective and antifibrotic effects of histidine in thioacetamide (TAA)-induced liver fibrosis in rats. This study was carried out on 100 Wistar Albino rats, classified into five groups, each containing 20 rats: Group I (control group), Group II: rats were given histidine intraperitoneally, Group III: rats were injected intraperitoneally with TAA, Group IV: rats were injected with L-histidine together with TAA, and Group V: rats were injected with TAA for 1 month then treated with intraperitoneal injection of L-histidine for another month. At the end of experiment, blood and liver were collected for determination of some liver enzymes, plasma total antioxidant capacity (TAC), serum ATX activity, and liver tissue hydroxyproline. Thioacetamide treatment caused significant increases in liver enzymes, ATX activities, and liver hydroxyproline, but a significant decrease in plasma's TAC. Upon treatment with histidine, a significant decrease in liver enzymes, ATX activities, and liver hydroxyproline was observed with a significant increase in plasma TAC in Group IV and a significant decrease in Group V. Histidine as an antioxidant has a protective effect on TAA-induced liver fibrosis; it is beneficial in rats not only by inhibition of collagen synthesis and increasing TAC but also by inhibition of ATX activities thus reducing its capacity to produce lysophosphatidic acid, which has a role in liver fibrosis.
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| http://dx.doi.org/10.1002/jbt.20370 | DOI Listing |
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