Targeting autophagy as a therapeutic strategy for identification of liganans from Peristrophe japonica in Parkinson’s disease

PD is characterized by the loss of dopaminergic neurons in substantia nigra, and the loss of dopamine resulting in motor deficit. 1 Its main pathological hallmarks include the genetic mutations of gene such as α-synuclein. 2 Increasing study showed that the dopaminergic neurons in midbrain are sensitive and damaged by the PD toxins. 6-Hydroxydopamine (6-OHDA) is widely used to induce lesion of nigrostriatal dopaminergic system in the PD model systems, including nerve cells, Caenorhabditis elegans ( C. elegans ), and rats. 3 Autophagy (mitophagy) is a cellular self-digestive process that engulfs the damaged organelles, including injured mitochondria and misfolded proteins such as α-synuclein. 4 Therefore, enhanced autophagy plays an important role in neuroprotection via cellular degradation of damaged mitochondria or mutant proteins in neurodegenerative diseases such as PD. Peristrophe japonica (PJ), a traditional Chinese medicine, is reported to exhibit anti-inflammatory, anti-bacterial, and anti-oxidative effects. 5 However, the neuroprotective components of PJ and the mechanism remain un-elucidated.

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