Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
Board

We have demonstrated in this work that G-115 extracted from Panax ginseng and the total saponin extract from the Panax quinquefolius elicited different vascular effects: G-115 having more prominent inhibitory action on PE-induced response without much effect on KCl-induced vascular contraction. PQS, on the other hand, exerted more inhibitory action on KCl-induced contraction than PE-induced contraction. This observation is interesting in a number of aspects, which are discussed below.

We have previously compared the vascular effects of the total ginsenosides isolated from Panax notoginseng (PNS) and the ginsenosides isolated from Panax quinquefolius (PQS) isolated chromatographically according to Shibata et al. (1983). We observed that PNS caused an inhibition of the contraction induced by sub-optimal concentration of PE, whereas PQS caused a further stimulation of contraction induced by sub-optimal concentrations of PE (Kwan 1996). Neither preparation of the ginsenosides affected KCl-induced contraction. From the viewpoint of traditional Chinese herbal therapy, it is interesting to note that Panax notoginseng and Panax quinquefolius are of opposite nature; the former being “cool” and the latter being “warm” in nature. According to the yin-yang principle of the traditional Chinese medical writing, herbs of cool nature are used to treat illness due to excess in “yang” forces and herbs of warm nature are used to treat excess in “yin” forces. The opposite effects of PNS (inhibitory) and PQS (stimulatory) of PE-induced vascular contraction seem to coincide with its traditional categorization of the use of ginseng plants. Like Panax notoginsneg, Panax ginseng is considered “warm” by Chinese herbalist. The similar vascular effects of G-115 and PNS also appear to be consistent along this line of thoughts.

The differential vascular effects of G-115 and PQS reported in the present study could be due to the use of different vascular tissues, since the same preparation of ginsenosides has been shown to cause different effects; i.e., vasodilatation vs vasoconstriction (Chen et al. 1984). However, the vasodilatory effect of PNS does not seem to be dependent on the blood vessel used as similar inhibitory effects were observed in rabbit aorta, dog mesenteric arteries and dog sephanous veins (Guan et al. 1985, 1994, Kwan et al. 1988). The early variable results obtained from these Panax ginseng preparations may also be due to their effects on the endothelial cells, which were not recognized at the time (Gillis 1997). Indeed, the ginsenosides from Panax ginseng as well as from other ginseng species are well known to have free radical scavenging properties (Zhang et al. 1996) by virtue of their antioxidant actions (Gillis 1997), which may account for their effectiveness in tissue protection against ischemia-reperfusion induced injury (Kim et al. 1992, Zhang and Liu 1994, Zhan et al. 1994). It is possible that these actions may be linked to their differential actions on the release of vasoactive substances from the endothelial cells, as the vascular endothelial cell is an early target of free radical injury in the cardiovascular system (Jackson et al., 1986). Kang et al. (1995) reported that ginsenosides of the protopanaxatriol group cause endothelium-dependent relaxation in the rat aorta. The relaxation effect of rat aorta observed in this study is unlikely to be endothelium-dependent, because only the endothelium-denuded preparation was employed in this work.

The information on the vascular effects of PQS appears to be quite limited. It is interesting to note that the PQS prepared from the ginseng root enhanced the contraction induced by sub-optimal concentrations of PE, but had no effect on KCl-induced contraction (Kwan 1996). However, in this study, the PQS extracted from the stems and leaves was shown to inhibit KCl-induced contraction and had only a small inhibitory effect on PE-induced contraction. Wu et al. (1995) also showed that PQS of the stems and leaves equally antagonized the contractions induced by KCl and norepinephrine in a non-competitive manner. These studies collectively confirmed that the vascular effects of ginsenosides depend on the part of the plant from which the ginsenosides are extracted (Liberti and Marderosian 1978).

Other than the antioxidant actions, some ginsenosides also possess Ca2+ antagonistic actions in a number of cell types (Kimura et al. 1988, Xiong et al. 1989, Teng et al. 1989; Guan et al. 1988, Zhang et al. 1994, Jiang et al. 1996). The selective inhibition by PNS (and also G-115) on PE-induced vascular contraction and the lack of its effect on KCl-induced contraction suggested a unique actions on the putative receptor-operated Ca2+ channels in vascular smooth muscle (Guan et al. 1985,1988, 1994). However, the direct effect of ginsenosides on the Ca2+ channels is yet to be demonstrated.

Back to the top.