Neuroprotective effect of Cistanche deserticola glycosides in MPTP-Induced Parkinson's disease mouse model involves Nrf2 activation.

Abstract

Parkinson's Disease (PD) a progressive neurodegenerative disorder is attributed to dopaminergic neuronal cell loss in the mid-brain substantia nigra pars compacta. A major risk factors associated with PD development is presence of excess oxidative stress. Previously, glycosides derived from Cistanche deserticola were reported to play a key role in counteracting PD; however, the underlying mechanisms remain to be determined. This study aimed to examine the neuroprotective effect attributed to glycosides derived from C. deserticola in PD model in mice. The model of PD was established by injecting intraperitoneally 1-methyl-4-penyl-1,2,3,6-tetrahydropyridine (MPTP). Rotarod and pole tests determined neurological behavior. The following immunohistochemistry, and metabolic biomarkers were measured mid-brain substantia nigra: (1) number of dopaminergic neuronal cell using immunohistochemistry (2) oxidative stress as evidenced by activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well levels of malondialdehyde (MDA), (3) inflammatory infiltration as measured by levels of IL-1β and TNF-α (4) by Western blot involvement of protein expression levels of Nrf2 signaling pathway. Data demonstrated that C. deserticola glycosides treatment improved behavioral performance, increased number of dopaminergic neurons, reduced cytokine levels of IL-1β and TNF-α accompanied by enhanced antioxidant activity in PD mice. These observations were associated with activation of Nrf2 signaling pathway. Data suggest that C. deserticola glycosides may thus be considered as an alternative compound for PD treatment.