Myricitrin alleviates MPP⁺-induced mitochondrial dysfunction in a DJ-1-dependent manner in SN4741 cells.

Oxidative stress and mitochondrial dysfunction have been linked to Parkinson's disease. DJ-1 is a recessive familial PD gene involved in antioxidative function and mitochondrial maintenance. Myricitrin, a flavanoid isolated from the root bark of Myrica cerifera, has potent antioxidative properties. In the present study, we investigated the protective effects of myricitrin against MPP(+)-induced mitochondrial dysfunction in SN4741 cells and attempted to elucidate the mechanisms underlying this protection. The results showed that incubating SN4741 cells with myricitrin significantly reduced cell death induced by the neurotoxin MPP(+). Furthermore, myricitrin protected cells from MPP(+)-induced effects on mitochondrial morphology and function. However, these protective effects were lost under DJ-1-deficient conditions. Thus, our results suggest that myricitrin alleviates MPP(+)-induced mitochondrial dysfunction and increases cell viability via DJ-1, indicating that myricitrin is a potential beneficial agent for age-related neurodegenerative diseases, particularly Parkinson's disease.