Elucidating the Neuroprotective Role of Formulated Camel α-Lactalbumin-Oleic Acid Complex by Curating the SIRT1 Pathway in Parkinson's Disease Model.

Abstract

Parkinson's Disease (PD) is characterized by increased oxidative stress and decreased level of dopamine. At present, the therapeutic interventions of PD are associated with undesirable adverse effects. To overcome these side effects, a new candidate bioinspired molecule is needed for the management of PD. Camel α-lactalbumin (α-LA) is the most abundant protein in camel's milk and has a potential to act as a nutraceutical supplement for neurological functions. Oleic acid, a monounsaturated fatty acid, has been widely associated with a reduced risk of PD. The present study aimed to formulate the camel α-LA and oleic acid (CLOA) complex under specific conditions and to evaluate its efficacy as a neuroprotective in rotenone induced PC12 cell model of PD. Our results demonstrated that removal of Ca++ ions from camel α-LA by EDTA enhances its binding efficiency with oleic acid, and the complex was characterized by UV-CD, ANS fluorescence spectroscopy, and NMR spectroscopy. Moreover, CLOA complex treatment reduced the oxidative stress and increased the cell viability by enhancing the level of dopamine and the expression of SIRT1, FOXO3a, HIF-1α, and HSF-1. We also validated the neuroprotective role of the complex by incubating the cells with CLOA complex prior to rotenone treatment. We inferred from the outcome of the results that the individual entity, i.e., α-LA or OA, is not as effective as the complex. Taken together, our study indicates that CLOA complex might be a potential candidate for the development of future therapeutic drugs for PD.