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. 2012 Jan;36(1):16-26.
doi: 10.5142/jgr.2012.36.1.16.

Cardiovascular Diseases and Panax ginseng: A Review on Molecular Mechanisms and Medical Applications

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Cardiovascular Diseases and Panax ginseng: A Review on Molecular Mechanisms and Medical Applications

Jong-Hoon Kim. J Ginseng Res. 2012 Jan.

Abstract

Ginseng is one of the most widely used herbal medicines and is reported to have a wide range of therapeutic and pharmacological applications. Ginseng may also be potentially valuable in treating cardiovascular diseases. Research concerning cardiovascular disease is focusing on purified individual ginsenoside constituents of ginseng to reveal specific mechanisms instead of using whole ginseng extracts. The most commonly studied ginsenosides are Rb1, Rg1, Rg3, Rh1, Re, and Rd. The molecular mechanisms and medical applications of ginsenosides in the treatment of cardiovascular disease have attracted much attention and been the subject of numerous publications. Here, we review the current literature on the myriad pharmacological functions and the potential benefits of ginseng in this area. In vitro investigations using cell cultures and in vivo animal models have indicated ginseng's potential cardiovascular benefits through diverse mechanisms that include antioxidation, modifying vasomotor function, reducing platelet adhesion, influencing ion channels, altering autonomic neurotransmitters release, and improving lipid profiles. Some 40 ginsenosides have been identified. Each may have different effects in pharmacology and mechanisms due to their different chemical structures. This review also summarizes results of relevant clinical trials regarding the cardiovascular effects of ginseng, particularly in the management of hypertension and improving cardiovascular function.

Keywords: Antioxidants; Cardiovascular disease(CVD); Lipid profile; Myocardial ischemia; Panax ginseng; Vasomotor tone.

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Figures

Fig. 1.
Fig. 1.. Pathway relating cardiovascular disease (CVD) mortality. The established CVD risk factors lie in the middle of a chain of events that leads to cardiac death.
Fig. 2.
Fig. 2.. Role of sodium- and calcium-overload in the pathogenesis of hypercontracture after cardiac ischemia/reperfusion.

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