Korean Red Ginseng and Rb1 facilitate remyelination after cuprizone diet-induced demyelination

Brain plasticity and ginseng

“…In Table 2 , recent literatures published within the past three years that can help to understand the molecular mechanisms through which ginseng acts in brain plasticity are summarized. Ginseng has influenced brain plasticity by affecting various cells within the central nervous system, including neurons [ 41 , 56 , [73] , [74] , [75] , [76] , [77] , [78] ], oligodendrocytes [ [79] , [80] , [81] , [82] ], astrocytes [ 83 , 84 ], microglia [ 82 , 85 ], and peripheral systems such as gut microbiota [ 69 , 70 , 86 ]. In terms of molecular level, the effects of ginseng have been observed in the altered levels of neurotransmitters (such as serotonin [ [73] , [74] , [75] , 86 ], dopamine [ 74 , 86 ], and gamma-aminobutyric acid (GABA) [ 73 ]), N-methyl- d -aspartate receptor (NMDAR) subunits [ 76 ], synaptic proteins [ 56 ], and Brain-Derived Neurotrophic Factor (BDNF) [ 56 , 73 , 74 ].…”

“… OL Mice Cuprizone model, In vitro (Primary OPC cultures) KRG Increased myelin gene expression. [ 81 ] Mitochondria, Proliferation N.A. Astrocyte Mice In vivo (male C57BL/6), In vitro (primary human brain astrocytes) KRG Number of astrocytes↑, Mitochondrial biogenesis↑ [ 83 ] Gap junction Depression Astrocyte Rats Chronic restraint stress KRG Depressive symptoms↓, Cx43↑ in PFC, astrocytes number↑, astrocyte gap junction function ↑ [ 84 ] Inflammation Memory Microglia Mice In vivo (Scopolamine-induced impairment), In vitro (BV2 cell line) Black ginseng-enriched Chong-Myung-Tang Memory ↑/Suppressed NO production, proinflammatory cytokine expression (iNOS, COX2, IL1b), NFkB pathway, MAPK pathway in BV2 cells.…”

“…In primary oligodendrocyte precursor cell (OPC) culture, gintonin, a fraction of ginseng [ 80 ], and the non-saponin fraction [ 79 ] promote OPC proliferation, while saponin fractions, especially Rb1, promote oligodendrocyte differentiation and myelin formation [ 79 ]. In an in vivo cuprizone demyelination model, administrations of KRG, Rb1 or Rg1 promoted the recovery of myelin or oligodendrocyte numbers [ 81 , 82 , 113 ]. Furthermore, in a chronic PD mouse model, Rg1 exhibited a protective role against lipid peroxidation stress in oligodendrocytes, protecting myelin sheaths and mature oligodendrocytes [ 114 ].…”