AI Article Synopsis
- Xylazine is increasingly being used as a street drug, leading to global cases of poisoning, but its long-term effects on liver health, specifically nonalcoholic fatty liver disease (NAFLD), are still unclear.
- In a study, rats given xylazine for 28 days showed weight loss and elevated liver enzymes, indicating liver damage; histopathological analysis confirmed the presence of steatosis, necrosis, and fibrosis in the liver.
- Genetic analysis revealed significant changes in gene expression linked to the PPAR signaling pathway, suggesting that this pathway is crucial in the development of xylazine-induced liver injury and NAFLD.
Article Abstract
With the gradual emergence of xylazine as a street drug, incidents of xylazine poisoning are now occurring worldwide. However, it remains unknown whether long-term exposure to xylazine causes nonalcoholic fatty liver disease (NAFLD). In the present study, the rats were injected with xylazine intraperitoneally for 28 consecutive days, and then serum and liver tissues were collected for analysis. Weight loss was observed in the 40 mg/kg group and elevated levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were observed. Histopathologic examination showed hepatic steatosis, necrosis, and fibrosis. By mRNA sequencing, 192 upregulated genes and 277 downregulated genes were found in the 40 mg/kg group, and the PPAR signaling pathway was ranked first in the KEGG pathway analysis. Four genes in the PPAR signaling pathway, Fabp5, Acox2, and Cpt2, were also verified in the 40 mg/kg group by RT-qPCR analysis and western blot. Our results demonstrated that long-term injection of xylazine causes NAFLD and the PPAR signaling pathway plays a core role in the process of xylazine-associated liver injury.
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| http://dx.doi.org/10.1002/jbt.70101 | DOI Listing |
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