Article Publish Status: FREE
Abstract Title:

and Its Active Principle Scopoletin Mitigate Protein Aggregation and Neuronal Apoptosis through Augmenting the DJ-1/Nrf2/ARE Signaling Pathway.

Abstract Source:

Oxid Med Cell Longev. 2019 ;2019:2761041. Epub 2019 May 2. PMID: 31191797

Abstract Author(s):

Kishore Kumar S Narasimhan, Deepthy Jayakumar, Prema Velusamy, Ashokkumar Srinivasan, Thangarajeswari Mohan, Divya Bhavani Ravi, Saraswathi Uthamaraman, Yogesh Kanna Sathyamoorthy, Namakkal Soorappan Rajasekaran, Kalaiselvi Periandavan

Article Affiliation:

Kishore Kumar S Narasimhan


Given the role of oxidative stress in PD pathogenesis and off-target side effects of currently available drugs, several natural phytochemicals seem to be promising in the management of PD. Here, we tested the hypothesis that scopoletin, an active principle obtained from(MC), efficiently quenches oxidative stress through DJ-1/Nrf2 signaling and ameliorates rotenone-induced PD. Despite reducing oxidative stress, the administration of MC extract (MCE) has lessened protein aggregation as evident from decreased levels of nitrotyrosine and-synuclein.studies revealed that scopoletin lessened rotenone-induced apoptosis in SH-SY5Y cells through preventing oxidative injury. Particularly, scopoletin markedly upregulated DJ-1, which then promoted the nuclear translocation of Nrf2 and transactivation of antioxidant genes. Furthermore, we found that scopoletin prevents the nuclear exportation of Nrf2 by reducing the levels of Keap1 and thereby enhancing the neuronal defense system. Overall, our findings suggest that scopoletin acts through DJ-1-mediated Nrf2 signaling to protect the brain from rotenone-induced oxidative stress and PD. Thus, we postulate that scopoletin could be a potential drug to treat PD.

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