Beneficial Effect of Vitamin E in Rotenone Induced Model of PD: Behavioural, Neurochemical and Biochemical Study

Abstract

Parkinson's disease (PD) a neurodegenerative disorder for which no preventive or long-term effective treatment strategies are available. Epidemiologic studies have failed to identify specific environmental, dietary or lifestyle risk factors for PD. However, oxidative stress in the SN is the most broadly accepted hypothesis for the etiopathology of PD. The Symptoms do not appear until there is a decline of striatal dopamine levels by 80% making it difficult to have early therapeutic interventions. Thus, the present experiment was designed to track down the sequential changes starting from the initiation of motor dysfunction and associated biochemical abnormality in rotenone based PD model. The study also evaluated the neuroprotective efficacy of vitamin E. Rats were treated with rotenone 2 mg/kg b.wt (s.c.) for 35 days. The level of dopamine decreased by 70~80% which was in turn reflected by marked deterioration in motor function such as (Total locomotor activity and catalepsy). Along with these the level of GSH and SOD declined significantly which was associated with elevated lipid peroxidation levels as much as by 60%.Vitamin E co-administration at a dose of 100 I.U/kg b.wt (i.m.) ameliorated rotenone induced changes in motor functions i.e Total locomotor activity and Catalepsy at the end of 5th week. Further, vitamin E supplementation significantly decreased lipid peroxidation and improved associated biochemical parameters i.e SOD and GSH level. Most interestingly the changes appeared as early as 3rd week suggesting that supplementation of vitamin E right at the beginning should be neuroprotective in PD.

Adenosine A2A Receptor Blockade Prevents Rotenone-Induced Motor Impairment in a Rat Model of Parkinsonism

“…Our results demonstrate that rotenone-treated rats exhibited motor deficits in the stride length and grid walking tests, as described by others (Hisahara and Shimohama, 2010 ; Li et al, 2012 ; von Wrangel et al, 2015 ), as well as lower dopamine levels in the midbrain (Höglinger et al, 2003 ; Sharma and Nehru, 2013 ), supporting its validity as a PD model. Notably, the A 2A R antagonist ZM241385 attenuated all these alterations induced by rotenone, whereas the A 1 receptor antagonist, DPCPX was devoid of effects.…”

Neuroprotective Effects of Pomegranate Juice against Parkinson’s Disease and Presence of Ellagitannins-Derived Metabolite—Urolithin A—In the Brain

“…Since bodyweight (b.w.) loss in animal rotenone models of PD has been demonstrated along with behavioral deficits, a loss of tyrosine hydroxylase (TH+) positive neurons of the SN, an increased apoptosis and a decreased antioxidant defense in the midbrain [30][31][32] we also monitored this parameter. In our study, exposure of rats to rotenone caused a significant decrease in b.w.…”

Nanomicellar formulation of coenzyme Q10 (Ubisol-Q10) effectively blocks ongoing neurodegeneration in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model: potential use as an adjuvant treatment in Parkinson's disease

“…for midbrain dopaminergic neurons and other neuronal and nonneuronal cell populations (Dumont and Beal, 2011;Ebadi et al, 1996;Fariss and Zhang, 2003;Koppula et al, 2012aKoppula et al, , 2012bMayo et al, 2005;Sharma and Nehru, 2013). However, the results of human clinical trials are inconsistent in slowing down disease progression, but there is still hope that improved antioxidant mimetics that better target ROS production pathways might prove beneficial.…”