Honey and levodopa comparably preserved substantia nigra pars compacta neurons through the modulation of nuclear factor erythroid 2-related factor 2 signaling pathway in 1-methyl-4-phenyl 1,2,3,6-tetrahydropyridine-induced Parkinson’s disease model

Parkinson’s disease (PD) affects about 8.5 million individuals worldwide. Oxidative and inflammatory cascades areimplicated in the neurological sequels, that are mostly unresolved in PD treatments. However, proper nutrition offers one of the mosteffective and least costly ways to decrease the burden of many diseases and their associated risk factors. Moreover, prevention maybe the best response to the progressive nature of PD, thus, the therapeutic novelty of honey and levodopa may be prospective. Thisstudy aimed to investigate the neuroprotective role of honey and levodopa against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced oxidative stress. Fifty-four adult male Swiss mice were divided into control and PD model groups of 27 mice. Eachthird of the control mice either received phosphate buffered saline, honey, or levodopa for 21 days. However, each third of the PDmodels was either pretreated with honey and levodopa or not pretreated. Behavioral studies and euthanasia were conducted 2 and8 days after MPTP administration respectively. The result showed that there were significantly (P<0.05) higher motor activities inthe PD models pretreated with the honey as well as levodopa. furthermore, the pretreatments protected the midbrain against thechromatolysis and astrogliosis induced by MPTP. The expression of antioxidant markers (glutathione [GSH] and nuclear factorerythroid 2-related factor 2 [Nrf2]) was also significantly upregulated in the pretreated PD models. It is thus concluded that honeyand levodopa comparably protected the substantia nigra pars compacta neurons against oxidative stress by modulating the Nrf2signaling molecule thereby increasing GSH level to prevent MPTP-induced oxidative stress.