Ginsenoside Rg1

Ginsenoside Rg1 (Rg1) activates promyogenic kinases, p38MAPK (mitogen-activated protein kinase) and Akt signaling, that in turn promotes the heterodimerization with MyoD and E proteins, resulting in enhancing myogenic differentiation. Through the activation of Akt/mammalian target of rapamycin pathway, Rg1 induces myotube growth and prevents dexamethasone-induced myotube atrophy. Furthermore, Rg1 increases MyoD-dependent myogenic conversion of fibroblast. Rg1 enhances glucose uptake in insulin-resistant myoblasts^[1]. Rg1 possesses the capacity for anti-aging activity in HSCs both in vitro and vivo^[2]. Ginsenoside Rg1 promotes endothelial progenitor cells (EPCs) adhesion, proliferation, migration and in vitro vasculogenesis in a dose- and time-dependent manner^[3]. Ginsenoside Rg1 could prevent cellular apoptosis via initiating an autophagic survival response, during which time Rg1 could promote the expression of Beclin1 and Bcl-2 and weaken the interaction between Beclin1 and Bcl-2^[4].

For the induction of myogenic differentiation, C2C12 cells are exchanged from growth medium (GM) containing 15% FBS to differentiation medium (DM) containing 2% HS. The efficiency of the myoblast differentiation is quantified. To induce hypertrophic myoblast differentiation, C2C12 cells are differentiated for 2 d and then treated with Rg1 for additional 2 days in DM. For the DEX-induced atrophy study, C2C12 cells are triggered to differentiate for 24 hrs and treated with 25 μM DEX and 10 nM Rg1, followed by incubation in DM for 2 days.

Rg1 can protect BMSCs against senescence and affect cell cycle phase distribution of bone marrow stromal cells (BMSCs) in aged rats. It affects inflammatory cytokine and stem cell factor (SCF) levels of BMSCs. Rg1 affects inflammatory cytokine and SCF levels of BMSCs. Rg1 improves the anti-aging ability of hematopoietic microenvironment through enhancing the anti-oxidant and anti-inflammatory capacities of BMSCs^[2]. Rg1 has neuroprotective properties in neurodegenerative diseases such as AD. Rg1 could ameliorate cognitive impairment in the mouse model of AD, improve the learning and memory abilities, decrease the levels of cerebral Aβ, maintain hippocampal neuron activity, and prevent cellular apoptosis induced by Aβ accumulation. On the other hand, Rg1 also could protect against brain aging by enhancing the scavenging of free radicals in the brain^[5].