Administration of quercetin improves mitochondria quality control and protects the neurons in 6-OHDA-lesioned Parkinson's disease models

Mounting evidence suggests that mitochondrial dysfunction and impaired mitophagy lead to Parkinson's disease (PD). Quercetin, one of the most abundant polyphenolic flavonoids, displays many health-promoting biological effects in many diseases. We explored the neuroprotective effect of quercetin in vivo in the 6-hydroxydopamine (6-OHDA)-lesioned rat model of PD and in vitro in 6-OHDA-treated PC12 cells. In vitro, we found that quercetin (20 mu M) treatment improved mitochondrial quality control, reduced oxidative stress, increased the levels of the mitophagy markers PINK1 and Parkin and decreased alpha-synuclein protein expression in 6-OHDA-treated PC12 cells. Moreover, our in vivo findings demonstrated that administration of quercetin also relieved 6-OHDA-induced progressive PD-like motor behaviors, mitigated neuronal death and reduced mitochondrial damage and alpha-synuclein accumulation in PD rats. Furthermore, the neuroprotective effect of quercetin was suppressed by knockdown of either Pink1 or Parkin.

Automated summary

Studies show that quercetin can improve mitochondrial quality control, reduce oxidative stress, increase levels of mitophagy markers PINK1 and Parkin, and decrease alpha-synuclein expression in 6-OHDA-treated cells. In vivo, quercetin also helps alleviate PD-like motor behaviors, decrease neuronal death, reduce mitochondrial damage, and control alpha-synuclein accumulation in PD rats. The neuroprotective effect of quercetin is compromised when either Pink1 or Parkin is knocked down.