AI Article Synopsis

  • Recent research indicates that Panax ginseng can positively impact cardiovascular health, particularly in relation to homocysteine (Hcy), which is linked to increased cardiovascular disease risk.
  • The study demonstrated that long-term treatment with ginseng saponins (GS) significantly reduced plasma Hcy levels and improved endothelial health in rats experiencing hyperhomocysteinemia due to L-methionine (Met).
  • Additionally, the combination of GS and Met led to reduced vasocontraction and enhanced vasodilation responses, suggesting GS may help mitigate vascular issues caused by high levels of Hcy.

Article Abstract

Recent studies have shown that Panax ginseng has a variety of beneficial effects on the cardiovascular systems. Homocysteine (Hcy), which is derived from L-methionine (Met), has been closely associated with the increased risk of cardiovascular diseases. In the present study, we examined whether in vivo long-term administration of ginseng saponins (GS), active ingredients of Panax ginseng, attenuate adverse vascular effects associated with chronic Met-induced hyperhomocysteinemia (H-Hcy). We found that plasma Hcy level, which was measured after 30 and 60 d, in GS (100 mg/kg)+Met co-administration group was significantly reduced when it was compared with Met alone treatment group. We could also observe the alleviation of endothelial damages of aortic artery vessels in GS (100 mg/kg)+Met co-administration group compared with Met alone treatment group. We compared aortic vasocontractile and vasodilatory responses between Met alone and GS (100 mg/kg)+Met co-treatment groups. We found that norepinephrine-induced vasocontractile responses were greatly decreased in GS (100 mg/kg)+Met co-treatment group and that carbachol-induced dilatory responses were greatly enhanced in GS (100 mg/kg)+Met co-administration groups as compared with Met alone treatment group. The present results indicate that in vivo long-term administration of GS attenuates adverse vascular effects associated with chronic Met-induced H-Hcy in rats.

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http://dx.doi.org/10.1248/bpb.29.2425DOI Listing

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