Confident relationships between diabetes and liver damagehave previously been established. This study was designed to evaluate hepatic inflammation, apoptosis, and endocannabinoid system alterations in diabetes with or without tropisetron treatment. Rats were assigned to five equal groups: control, tropisetron, diabetes, tropisetron+diabetes, and glibenclamide+diabetes (n = 7 in each group). Rats were treated with tropisetron (3 mg/kg) and glibenclamide (1 mg/kg) as a positive control for two weeks after type 1 diabetes induction.Inflammatory cytokines tumor necrosis factor-alpha and interleukin 6 (TNF-α and IL-6) levels, apoptotic cells, and fatty acid amide hydrolase (FAAH) enzyme, at both transcriptional and protein levels increased, while the gene expression of cannabinoid receptor 1 (CB1) and its protein level decreased in the diabetic liver compared to the control. Treatment with tropisetron reversed TNF-α, apoptotic index, and endocannabinoid system components. These effects were equipotent with glibenclamide, indicating that tropisetroncan protect liver tissue against diabetic disturbances. These findings strongly support the idea that diabetes-induced liver abnormality is mediated by inflammatory reactions, apoptosis, and endocannabinoid system, and that these effects can be alleviated by using tropisetron as an antioxidant and anti-inflammatory agent.
Copyright © 2019 Elsevier B.V. All rights reserved.
KEYWORDS: 5HT3 receptor, Apoptosis, Diabetes, Endocannabinoid system, Inflammation, Liver Injury, Metabolic diseases
- PMID: 31926479
- DOI: 10.1016/j.intimp.2019.106158