Abstract
Ginseng root is one of the most popular herbs throughout the world and it has been used as a medicine to enhance stamina and capacity to cope with fatigue and physical stress. In this study, we focused the cardiac protective effects of Compound K (C‐K; 20‐O‐D‐glucopyranosyl‐20(S)‐protopanaxadiol), which is a protopanaxadiol metabolite derived from ginsenoside Rb1, Rb2, and Rc by the metabolic actions of intestinal bacteria.Mice were exposed to 30 min ischemia followed by 120 min of reperfusion (control). Some mice were assigned to C‐K, or PI3K inhibitor, wortmannin. C‐K preconditioned significantly reduced infarct size compared to control group (22.4 ± 2.5% [n = 7] vs. 43.2 ± 2.0% [n = 12] respectively, p<0.05) and wortmannin eliminated the protection produced by C‐K (43.3 ± 2.4% [n = 7]). Additionally, the hearts treated with C‐K had a 2‐fold increase in basal phosphorylation of Akt and pretreated with wortmannin completely abolished Akt phosphorylation in response to C‐K treatment.These results reveal that C‐K produces cardiac protection in mice in association with PI3K/Akt signaling.
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