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Therapies targeting histone deacetylase (HDAC) have gainedwider attention in the treatment of various clinical conditions. However, theuse of HDAC inhibitors in pre-clinical trials in the case of Parkinson’s disease(PD) is very limited. In the present study, the HDAC inhibitor, entinostat, wastested in animals induced with Parkinson’s disease experimentally.    Material and methods  Wistar male rats (150 ±10 g) were administeredwith rotenone (2 mg/kg/day, s.c.) for 21 days to induce PD, while entinostat(20 mg/kg) was given intraperitoneally. Then, the neurological functions, PDmarkers, and HDACs were analysed in the control and experimental animals.    Results  The results demonstrated that rats that received entinostat displayed progressive motor, behavioural, and neurological function with attenuated α-synuclein and improved tyrosine-hydroxylase compared to controlcells. Moreover, the induction of PD in rats demonstrated reduced levels ofH2S, dopamine, 3, and 4-dihydroxyphenylacetic acid (DOPAC), and increasedmonoamine oxidase activity in PD rats. However, the rats that received entinostat demonstrated progressive levels of dopa and DOPAC, with attenuatedlevels of HDAC-2, -4, and -6 mRNA in the PD rats compared to controls. Onthe other hand, elevated (p &lt; 0.01) levels of PD marker genes such as GDF3and NMDA2b were reduced, with a significant increase in neuroprotectivegenes such as VDAC3 and CBX5 in entinostat-supplemented rats.    Conclusions  The study results suggest that inhibition of HDAC systematically improves the neurological functions, and hence treatments, emphasizing that HDACI, as the speculated mechanism, will be a promising mode oftreatment in PD.

Inhibition of histone deacetylase promotes a neuroprotective mechanism in an experimental model of Parkinson’s disease