Ginsenoside Rk3

Evid Based Complement Alternat Med. 2013;2013:690190.

Ginsenoside RK3 Prevents Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes via AKT and MAPK Pathway.[Pubmed: 23935671 ]

Cardiac hypertrophy is a thickening of the heart muscle that is associated with cardiovascular diseases such as hypertension and myocardial infarction. It occurs initially as an adaptive process against increased workloads and often leads to sudden arrhythmic deaths. Studies suggest that the lethal arrhythmia is attributed to hypertrophy-induced destabilization of cardiac electrical activity, especially the prolongation of the action potential. The reduced activity of Ito is demonstrated to be responsible for the ionic mechanism of prolonged action potential duration and arrhythmogeneity. Isosteviol (STV), a derivative of stevioside, plays a protective role in a variety of stress-induced cardiac diseases.
METHODS AND RESULTS:
Here we report effects of STV on rat ISO-induced hypertrophic cardiomyocytes. STV alleviated ISO-induced hypertrophy of cardiomyocytes by decreasing cell area of hypertrophied cardiomyocytes. STV application prevented the prolongation of action potential which was prominent in hypertrophied cells.
CONCLUSIONS:
The decrease and increase of current densities for Ito and ICaL observed in hypertrophied myocytes were both prevented by STV application. In addition, the results of qRT-PCR suggested that the changes of electrophysiological activity of Ito and ICaL are correlated to the alterations of the mRNA transcription level.

Food Funct . 2017 Oct 18;8(10):3723-3736.

Anticancer effects of ginsenoside Rk3 on non-small cell lung cancer cells: in vitro and in vivo[Pubmed: 28949353]

Abstract Ginsenoside Rk3 (Rk3) is present in the roots of processed Panax notoginseng herbs and it exerts anti-platelet aggregation, pro-immunogenic and cardioprotective effects. However, little is known regarding the anticancer activities of this compound, especially in lung cancer. This study was designed to investigate the anticancer effects of Rk3 on non-small cell lung cancer (NSCLC) cells and in an H460 xenograft tumor model. Our results showed that Rk3 reduced cell viability, inhibited both cell proliferation and colony formation, and induced G1 phase cell cycle arrest by downregulating the expression of cyclin D1 and CDK4 and upregulating the expression of P21. Rk3 also induced apoptosis in a concentration-dependent manner in H460 and A549 cells by Annexin V/PI staining, TUNEL assay and JC-1 staining, resulting in a change in the nuclear morphology. Moreover, Rk3 induced the activation of caspase-8, -9, and -3, promoted changes in mitochondrial membrane potential, decreased the expression of Bcl-2, increased the expression of Bax, and caused the release of cytochrome c, which indicated that the apoptosis-inducing effects of Rk3 were triggered via death receptor-mediated mitochondria-dependent pathways. Furthermore, Rk3 significantly inhibited the growth of H460 xenograft tumors without an obvious effect on the body weight of the treated mice. Histological analysis indicated that Rk3 inhibited tumor growth by altering the proliferation and morphology of tumor cells. In addition, we confirmed that Rk3 inhibited angiogenesis via CD34 staining and chick embryo chorioallantoic membrane (CAM) assay in vivo. Taken together, our findings revealed not only the anticancer effect of Rk3 on NSCLC cells but also a new promising therapeutic agent for human NSCLC.

Biol Pharm Bull. 2011;34(6):898-900.

Anti-complementary ginsenosides isolated from processed ginseng.[Pubmed: 21628891]

METHODS AND RESULTS:
As part of an ongoing search for immunomodulatory components aimed at the anti-complementary effect, ginsenosides isolated from processed ginseng were found to have inhibitory activity on complement activation through classical pathways. Activity-guided fractionation was used to isolate four ginsenosides, namely ginsenoside Rg₆, F₄, Rk₃, and Rh₄. Ginsenoside Rk₃ and Rh₄ had a 3 fold higher inhibition activity than rosmarinic acid which was used as a positive control while ginsenoside Rg₆ and F₄ showed only mild effects similar to that of the positive control.
CONCLUSIONS:
The results suggest that the activity of the corresponding ginsenosides may be increased by the glycosyl moiety at the C₆ position rather than the double bond conformation at C₂₀, and ginsenoside Rk₃ and Rh₄ could have a role in treating inflammatory diseases.