FIGURE 4.

Schematic diagram on ginsenoside-induced various ion channel and receptor regulations on cell surface membrane. Ginsenoside (i.e., ginsenoside Rg₃) actions on cell surface ion channels and receptors show several characteristics. First, ginsenoside shows various non-specific regulations of ion channels and receptors as illustrated here. However, overall actions of ginsenoside decrease the cellular excitability of excitable cells by inhibiting cation influx (i.e., Ca²⁺ and Na⁺ channel activity inhibitions or K⁺ channel activation and ligand-gated ion channel inhibitions such as 5-HT₃, nACh, and NMDA receptors), and by stimulating anion influx (i.e., GABA_A and glycine receptor channel activation). Second, ginsenoside-induced ion channel and receptor regulations achieve via interaction with ion channel pore, channel pore entryway, and share channel blocker or toxin biding sites through site-directed mutagenesis studies (Nah, 2014). Third, ginsenoside itself does not induce ion channel or receptor inhibition or activation at resting state, without preceding stimulations of ion channel or receptors by depolarization or receptor ligand treatment. Thus, the biological or pharmacological effects of ginsenoside could be observed when cells or organs are stimulated beyond normal state rather than receptor mediation like gintonin.