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.