Effects of Carvacrol on Cognitive Function and Apoptotic Gene Expression in Trimethyltin- Induced Hippocampal Injury in Rats

Objective: Trimethyltin (TMT) chloride is an organotin compound used in industry. It has been linked to generatingreactive oxygen species (ROS), inflammatory processes, and neuronal death. Carvacrol is a monoterpene phenolfound in the Lamiaceae plant family, modulating inflammatory conditions and necroptosis in neural tissue. This studyaimed to investigate the neuroprotective effects of carvacrol in a rat model of hippocampal neuronal injury inducedby TMT. Materials and Methods: In this experimental study, sixty male Wistar rats were randomly divided into five groups(n=12): group 1 receiving saline, group 2 received dimethyl sulfoxide (DMSO) as a vehicle for 21 days, group 3 receivinga single dose of TMT (8 mg/kg) and groups 4 and 5 receiving carvacrol 40 and 70 mg/kg daily for 21 days after a singledose of TMT. All injections were intraperitoneal (I.P.). Caspase-3, Bax, Bcl-2, and Bdnf gene expression and the numberof pyknotic neurons in the hippocampus were quantified. Spatial memory was assessed with a radial arm maze. Results: Statistical analysis of histological data revealed the carvacrol significantly attenuated cognitive dysfunction andthe number of pyknotic neurons in the hippocampal CA1 region of rats treated with TMT. Based on real-time polymerasechain reaction (PCR), carvacrol modulated the expression of genes involved in apoptosis (Bax and Caspase-3) andupregulated anti-apoptotic (Bcl-2) and brain derived neurotrophic factor (Bdnf) genes in the hippocampal tissue. Conclusion: These findings revealed neuroprotective effects of carvacrol which might be mediated by apoptotic andanti-apopetotic factors.