Therapeutic potential of ginsenoside Rg3 and Rf for Huntington’s disease

• Published in: In vitro cellular & developmental biology. Animal Vol. 57; no. 6; pp. 641 - 648
• Main Authors: Lee, Mijung, Ban, Jae-Jun, Won, Bo Hee, Im, Wooseok, Kim, Manho
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.06.2021; Society for In Vitro Biology
• Subjects: Agglomeration; Animal Genetics and Genomics; Apoptosis; Apoptosis - drug effects; Biomedical and Life Sciences; Biosynthesis; Brain - drug effects; Caspase-3; Cell Biology; Cell Culture; Cell Survival - drug effects; Cell viability; Central nervous system; Cyclic AMP response element-binding protein; Developmental Biology; Genetic disorders; Ginseng; Ginsenosides; Ginsenosides - pharmacology; Health services; Herbal medicine; Humans; Huntingtin; Huntingtin Protein - genetics; Huntington Disease - drug therapy; Huntington Disease - genetics; Huntington Disease - pathology; Huntington's disease; Huntingtons disease; Immunocytochemistry; Life Sciences; Mitochondria; Mutant Proteins - genetics; Neural stem cells; Neural Stem Cells - drug effects; p53 Protein; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha - genetics; Phenotypes; Stem cell transplantation; Stem Cells; Mutant huntingtin; Huntington’s disease; Ginseng; Ginsenoside
• ISSN: 1071-2690; 1543-706X
• DOI: 10.1007/s11626-021-00595-1

Ginseng is a popular herbal medicine and known to have protective and therapeutic effects in various diseases. Ginsenosides are active gradients representing the diverse pharmacological efficacy of ginseng. Huntington’s disease (HD) is incurable genetic disorder associated with mutant huntingtin (mHtt) aggregation in the central nervous system. This study was conducted to investigate the effects of ginsenoside Rg3 and Rf on mHtt aggregation, cell viability, mitochondrial function, and apoptotic molecules on HD model. To investigate the effect of ginsenosides on HD, neural stem cells were isolated from the R6/2 mouse brain and used as a cellular model of HD. Nuclear aggregation of mHtt was measured by immunocytochemistry, and expressions of mitochondrial biogenesis and apoptotic molecules were investigated by western blot. As a result, the number of mHtt aggregates positive cells has decreased by ginsenoside Rg3 and Rf treatment in cellular model of HD. Mitochondrial biogenesis-related molecules such as PGC-1α and phosphorylated CREB were increased or showed increased tendency by ginsenoside Rg3 and Rf. Apoptotic molecules, p53, Bax, and cleaved caspase-3, were down-regulated by treatment of ginsenoside Rg3 and Rf. In addition, Lysotracker staining result showed that cellular lysosomal content was reduced by ginsenoside Rg3 and Rf. Given that ginsenoside Rg3 and Rf have the potential to reduce mHtt aggregation and cellular apoptosis, these ginsenosides can be possible therapeutic candidates for treating HD phenotypes.