Monascin exhibits neuroprotective effects in rotenone model of Parkinson's disease via antioxidation and anti-neuroinflammation.

Increasing evidence verified that oxidative stress and neuroinflammatory response exacerbates motor deficits and increases neuronal loss in several rodent models of Parkinson's disease. In the present study, we explore the neuroprotective effects of monascin in a rotenone-induced Parkinson's disease model as well as the underlying mechanisms. Our results showed that monascin remarkedly attenuated behavioral impairments and the depletion of dopaminergic neurons induced by rotenone in the rats. Besides, monascin decreased the levels of pro-inflammatory factors such as interleukin-1β, interleukin-6, tumor necrosis factor-α and oxidative stress marker malondialdehyde while promoted the expression of superoxide dismutase, glutathione peroxidase and other antioxidant factors. Further detection of the expression of related proteins showed that monascin significantly promoted the expression of proliferator-activated receptor-gamma, F-E2-related factor 2 and heme oxygenase-1, but inhibited the expression of NF-κB. What's more, levels of growth factors that are essential for neuronal and synaptic function were increased under the effects of monascin. All in all, our results revealed that monascin exerted neuroprotective effects in rotenone model of Parkinson's disease via antioxidation and anti-neuroinflammation.