cinnamaldehyde attenuates dopaminergic neuronal loss in substantia nigra and induces midbrain catalase activity in a mouse model of parkinson’s disease

Background and objective: parkinson's disease (pd) is the second most common neurodegenerative disease after alzheimer's disease that affects 3% of the population. pd involves a progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta (snc) and subsequent loss of dopamine. dopamine depletion leads to movement dysfunction and is accompanied with tremor, rigid muscles and impaired balance. mechanisms of the pathogenesis of pd include oxidative stress and inflammation. cinnamaldehyde acts as a powerful antioxidant and anti-inflammatory agent. this research is focused on the effects of cinnamaldehyde on neurons of snc of mouse model of pd. materials and methods: adult male mice with an average weight of 25-35 g were divided into 4 groups of 5 each: group 1: control pbs, group2: mptp, group 3: mptp + cinnamaldehyde pretreatment (30 mg/kg), and group 4: mptp + cinnamaldehyde treatment (30 mg/kg). rotarod test was used to assess motor and balance of the mice. after behavioral studies, all the mice were anesthetized and perfused transcardially with 0.1 m pbs (ph=7.4) followed by 4% buffered paraformaldehyde fixative. the brains of the mice were removed and fixed in the paraformaldehyde and stained for tunel and ihc. then the number of the apoptotic, th+ and gfap+ cells were counted. the level of mda and catalase enzyme activity were also evaluated. data was analyzed using spss software by one way of variance (anova) and t-test. results: the results showed that groups 3 and 4 had significantly better locomotion than group 2 (p<0.05). cinnamaldehyde also induced catalase enzyme activity and significantly decreased the number of apoptotic neurons in snc in groups 3 and 4 as compared to group 2 (p<0.05). conclusion: this study showed that cinnamaldehyde attenuates dopaminergic neuronal loss in substantia nigra and induces midbrain catalase activity in a mouse model of parkinson’s disease.