Benefits of Betanin in Rotenone-Induced Parkinson Mice

Abstract

The present study aimed to investigate betanin’s neuroprotective effect in mice with rotenone-induced Parkinson-like motor dysfunction and neurodegeneration. Forty male ICR mice were divided into 4 groups: Sham-veh, Rot-veh, Rot-Bet100 and Rot-Bet200. Rotenone (Rot) at 2.5 mg/kg/48 h was subcutaneous injected, and betanin (Bet) at 100 and 200 mg/kg/48 h were given alternately with the Rot injections in Rot-Bet groups for 6 weeks. Motor dysfunctions were evaluated weekly using hanging wire and rotarod tests. Malondialdehyde (MDA), reduced glutathione (GSH), catalase (CAT), superoxide dismutase (SOD), neuronal degeneration in the motor cortex (MC), striatum (Str) and substantia nigra par compacta (SNc) were evaluated. The immunohistochemical densities of tyrosine hydroxylase (TH) in Str and in SNc were also measured. We found that rotenone significantly decreased the time to fall in a hanging wire test after the 4th week and after the rotarod test at the 6th week (p<0.05). The percentage of neuronal degeneration in MC, Str and SNc (p<0.05) significantly increased, and the TH density in Str and in SNc (p<0.05) significantly decreased. Betanin at 100 and 200 mg/kg significantly prevented MC, Str and SNc neuronal degeneration (p<0.05) and prevented the decrease of TH density in Str and in SNc (p<0.05). These findings appeared concurrently with improved effects on the time to fall in hanging wire and rotarod tests (p<0.05). Treatment with betanin significantly prevented increased MDA levels and boosted GSH, CAT and SOD activities (p<0.05). Betanin exhibits neuroprotective effects against rotenone-induced Parkinson in mice regarding both motor dysfunction and neurodegeneration. Betanin’s neurohealth benefit relates to its powerful antioxidative property. Therefore, betanin use in neurodegenerative disease therapy is interesting to study.

Neuroprotective effects of betanin in mice with cerebral ischemia-reperfusion injury

“…Hydroxyl radicals as a cascade product originating from O2can exacerbate damage via lipid peroxidation, as indicated by an increased MDA level during IR [33]. Similar to other studies, we showed that IR led to increased MDA and that betanin helped reduce MDA [9,17,34]. Betanin inhibited this toxic metabolite of lipid peroxidation, depending on its cyclic amine and hydroxyl groups, which act as good hydrogen and electron donors [35].…”

“…Betanin's neuroprotective efficacy includes its potent antioxidative properties, such as its inhibitory effect on lipid peroxidation by attenuation of malondialdehyde (MDA) levels. Betanin also helped reduced glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD) activities [9,10]. Dugger and Dickson [11] found evidence of many pathomechanism-joining degenerative diseases, such as oxidative stress and inflammation.…”