Stability of angiogenic agents, ginsenoside Rg1 and Re, isolated from Panax ginseng: In vitro and in vivo studies

Development of inhalable dry powder formulation of basic fibroblast growth factor

“…First, bFGF has four cysteine residues, which are highly reactive under oxidative conditions (Caccia et al, 1992). Its stability is also negatively affected by heat, organic solvent, and pH (Yu et al, 2007). Second, since the anticipated bFGF dose per inhalation is in the microgram range (Jeon et al, 2007), the use of inactive excipients is inevitable.…”

“…Here, we used the spray-drying method to prepare inhalable dry powders containing bFGF and studied the effects of carrier excipients on the aerodynamic properties of the dry powder and the integrity of bFGF. The results of our study show that, albeit the poor stability profile (Caccia et al, 1992;Yu et al, 2007), bFGF can be successfully formulated as an inhalable powder when the carrier excipients are judiciously selected.…”

Ginseng total saponins enhance neurogenesis after focal cerebral ischemia

“…The mechanisms might be as follows: (A) GTS are important neuron protective factors, which can increase the expression of brain-derived neurotrophic factors and the plasticity-related proteins, as well as Bcl-2 and antioxidant enzymes, enhance new synapse formation, and inhibit apoptosis and calcium overload (Salim et al, 1997;Cheng et al, 2005;Yuan et al, 2007;Zhao et al, 2009); (B) GTS can promote expression of VEGF, bFGF, etc. And through stimulating angiogenesis (Sengupta et al, 2004;Yue et al, 2005;Kim et al, 2007;Leung et al, 2007;Yu et al, 2007) and increasing regional cerebral blood flow, GTS can protect brain tissue against ischemic injury; (C) most importantly, GTS might directly induce endogenous NSCs to proliferate and further differentiate into neuron-like cells and to replace the necrotic cells. However, the possible specific mechanisms by which GTS enhance neurogenesis and promote the recovery of neurological function after cerebral infarction still need further elucidation.…”

Ginsenoside Rg1 promotes endothelial progenitor cell migration and proliferation

“…They both possess four trans-ring rigid steroid skeletons with a modified side-chain at C20, which is absent in estradiol [8] . Re and Rg1 may be a novel group of non-peptidic angiogenic agents with superior stability and may be used for the management of tissue regeneration [38] . BMSC proliferation stimulated by ginsenoside Rg1 can be completely blocked by ER antagonist ICI 182, 780, or ERα-specific antagonist methylpiperidinopyrazole, which indicates that ERα may be the key subunit that enables Rg1 to exert its action on BMSC [39] .…”