Research Papers: Gerotarget (Focus on Aging):

Autophagy flux induced by ginsenoside-Rg3 attenuates human prion protein-mediated neurotoxicity and mitochondrial dysfunction

Ji-Hong Moon _, Ju-Hee Lee, You-Jin Lee and Sang-Youel Park

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Oncotarget. 2016; 7:85697-85708. https://doi.org/10.18632/oncotarget.13730

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Ji-Hong Moon1, Ju-Hee Lee1, You-Jin Lee1 and Sang-Youel Park1

1 Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan, Jeonbuk, South Korea

Correspondence to:

Sang-Youel Park, email:

You-Jin Lee, email:

Keywords: ginsenoside Rg3; autophagy; neuron; mitochondria; prion; Gerotarget

Received: April 08, 2016 Accepted: November 11, 2016 Published: November 30, 2016


Mitochondrial quality control is a process by which mitochondria undergo successive rounds of fusion and fission with dynamic exchange of components to segregate functional and damaged elements. Removal of mitochondrion that contains damaged components is accomplished via autophagy. In this study, we investigated whether ginsenoside Rg3, an active ingredient of the herbal medicine ginseng that is used as a tonic and restorative agent, could attenuate prion peptide, PrP (106-126)-induced neurotoxicity and mitochondrial damage. To this end, western blot and GFP-LC3B puncta assay were performed to monitor autophagy flux in neuronal cells; LC3B-II protein level was found to increase after Rg3 treatment. In addition, electron microscopy analysis showed that Rg3 enhanced autophagic vacuoles in neuronal cells. By using autophagy inhibitors wortmannin and 3-methyladenine (3MA) or autophagy protein 5 (Atg5) small interfering RNA (siRNA), we demonstrated that Rg3 could protect neurons against PrP (106-126)-induced cytotoxicity via autophagy flux. We found that Rg3 could also attenuate PrP (106-126)-induced mitochondrial damage via autophagy flux. Taken together, our results suggest that Rg3 is a possible therapeutic agent in neurodegenerative disorders, including prion diseases.

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