Ginsenosides that produce differential antinociception in mice

Intrathecal treatments with ginsenosides produce antinociceptive effect on proinflammatory cytokines-induced pain behavior in mice

“…Several lines of evidence have previously demonstrated that ginsenosides are the major active components of ginseng and exert their antinociceptive effects when they are administered orally or centrally (Suh et al 1997(Suh et al , 1999Mogil et al 1998;Yoon et al 1998;Shin et al 1999;Nah et al 2000;Rhim et al 2002;Choi et al 2003a). Now, we found in the present study that several ginsenosides such as R b1 , R b2 , R c , R f , R g1 , and R g3 administered spinally reduce the pain behavior elicited by pro-inflammatory cytokines such as TNF-a, IL-1b, or IFN-g administered spinally.…”

“…or intrathecal (i.t.) modulate nociception in several pain models (Suh et al 1997(Suh et al , 1999Mogil et al 1998;Yoon et al 1998;Shin et al 1999;Nah et al 2000;Rhim et al 2002;Choi et al 2003a). Spinal administration with ginsenosides inhibits antinociception induced by morphine (a mu opioid receptor agonist) or U-50,488H (a kappa opioid receptor agonist) in mice (Kim et al 1992;Suh et al 1997Suh et al , 2000.…”

“…In addition, some ginsenosides modulate pain transmission processing in inflammationinduced pain model. For example, formalin-induced pain behavior is inhibited by some ginsenosides such as R c , R d , and R e (Shin et al 1999). Furthermore, the same ginsenosides are effective for ameliorating pain behavior elicited by intraperitoneal injection with acetic acid (Shin et al 1999).…”

“…For example, formalin-induced pain behavior is inhibited by some ginsenosides such as R c , R d , and R e (Shin et al 1999). Furthermore, the same ginsenosides are effective for ameliorating pain behavior elicited by intraperitoneal injection with acetic acid (Shin et al 1999). Moreover, we have previously demonstrated that pain behaviors induced by spinally administered substance P, one of the neurotransmitters responsible for pain transmission at the spinal cord level (Hunt & Mantyh 2001), are also inhibited by some ginsenosides (Choi et al 2003a).…”

“…Some groups found that pro-inflammatory cytokines play important roles in the production or regulation of hyperalgesia or allodynia (Watkins et al 1994;Tadano et al 1999;Reeve et al 2000). Several lines of evidence have shown that ginsenosides can modulate inflammationinduced pain processing (Mogil et al 1998;Yoon et al 1998;Shin et al 1999;Nah et al 2000;Choi et al 2003a). We have previously reported that some of ginsenosides administered supraspinally reduce the pain behaviors induced by pro-inflammatory cytokines (Seo et al 2008).…”