Thymol protects against 6-hydroxydopamine-induced neurotoxicity in in vivo and in vitro model of Parkinson's disease via inhibiting oxidative stress.

BACKGROUND: Parkinson's disease (PD) is a multifactorial movement disorder with the progressive degeneration of the nigrostriatal system that impairs patients' movement ability. Oxidative stress has been found to affect the etiology and pathogenesis of PD. Thymol, a monoterpenic phenol, is one of the most important dietary constituents in thyme species. It has been used in traditional medicine and possesses some properties including antioxidant, free radical scavenging, anti-inflammatory. In this study, in vitro and in vivo experiments were performed with the thymol in order to investigate its potential neuroprotective effects in models of PD. METHODS: The present study aimed to evaluate the therapeutic potential of thymol in 6-hydroxydopamine (6-OHDA)-induced cellular and animal models of PD.  RESULTS: Post-treatment with thymol in vitro was found to protect PC12 cells from toxicity induced by 6-OHDA administration in a dose-dependent manner by (1) increasing cell viability and (2) reduction in intracellular reactive oxygen species, intracellular lipid peroxidation, and annexin-positive cells. In vivo, post-treatment with thymol was protective against neurodegenerative phenotypes associated with systemic administration of 6-OHDA. Results indicated that thymol improved the locomotor activity, catalepsy, akinesia, bradykinesia, and motor coordination and reduced the apomorphine-caused rotation in 6-OHDA-stimulated rats. Increased level of reduced glutathione content and a decreased level of MDA (malondialdehyde) in striatum were observed in the 6-OHDA rats post-treated with thymol. CONCLUSIONS: Collectively, our findings suggest that thymol exerts protective effects, possibly related to an anti-oxidation mechanism, in these in vitro and in vivo models of Parkinson's disease.

Neurogenesis in the rat neonate's hippocampus with maternal short-term REM sleep deprivation restores by royal jelly treatment.

BACKGROUND: Numerous studies have shown the effects of rapid eye movement sleep deprivation (REM-SD) on behavior and brain structures. The impact of REM-SD on learning and memory, thus neurogenesis, has been reported in previous studies. Royal jelly (RJ) is known as the wealthiest biological nutrient with various physiological properties. This study aimed to study the possible effect of RJ on neurogenesis of the rat hippocampus neonates following exposure of mother to REM-SD during pregnancy. METHODS: Thirty neonate rats from 15 pregnant Wistar rats were used. To induce REM-SD, the flowerpot method was used. The pregnant rats were divided into five groups (n = 3): group 1, no treatment; group 2, REM-SD; groups 3, 4, and 5, REM-SD +RJ. The former group received 72 h REM-SD during pregnancy (days 7, 14, 21), and the latter group received REM-SD + RJ (three trial groups). At week 4, the rat neonates of all groups were sacrificed (n = 6 each group). Their brains were fixed, removed, and prepared for Nissl and Hoechst 33342 staining. By using real time polymerase chain reaction methode the brain-derived neurotrophic factor BDNF gene expression was studied (RT-PCR), brain-derived neurotrophic factor (BDNF) gene expression was studied. The results were analyzed statistically, and the Pv  < .05 was considered significant. RESULTS: The results showed a significant decrease in the number of neurons in the hippocampus of neonatal rats of REM-SD mothers compared to the neonates of the mother with REM-SD + RJ. REM-SD also led to an increase in apoptosis reaching the neonates from the REM-SD + RJ animals. High expression of BDNF was observed in the hippocampus of the neonates from REM-SD + RJ treated mothers. CONCLUSION: RJ acts as a neuroprotective agent that could compensate for the effects of REM-SD on learning and memory via restoring neurogenesis.