KRGE regulated the expression of genes associated with abnormal physiology via HFD. Leptin, insulin, and adiponectin, which carry out critical functions in energy and lipid metabolism, were shown to be modulated by KRGE. These results show that KRGE is effective in preventing obesity.

Korean red ginseng has shown therapeutic effects for a number of disease conditions. However, little is known about the antiinflammatory effect of Korean red ginseng saponin fraction (RGSF) in vitro and in vivo. Therefore, in this study, we showed that RGSF containing 20(S)-protopanaxadiol type saponins inhibited nitric oxide production and attenuated the release of tumor necrotic factor (TNF)-α, interleukin (IL)-6, granulocyte monocyte colony stimulating factor (GMCSF), and macrophage chemo-attractant protein-1 in lipopolysaccharide (LPS) stimulated murine macrophage RAW264.7 cells. Moreover, RGSF down-regulated the mRNA expressions of inducible nitric oxide synthase, cyclooxyginase-2, IL-1β, TNF-α, GMCSF, and IL-6. Furthermore, RGSF reduced the level of TNF-α in the serum and protected mice against LPS mediated endotoxic shock. In conclusion, these results indicated that ginsenosides from RGSF and their metabolites could be potential sources of therapeutic agents against inflammation.

We have studied the effect of dietary supplementation with 25 mg (0.0025% of the total diet) of a lipophilic fraction (LF) from Panax ginseng on rat platelet aggregation induced by collagen or thrombin, and on blood coagulation. When platelets prepared from 15% corn oil plus LF-administered rats (COLF) were stimulated by thrombin (0.1 units/ml) and collagen (100 micrograms/ml), the cGMP level was significantly increased as compared with those from 15% corn oil only-administered rats (CO). The levels of cAMP in COLF were decreased by thrombin, but was increased by collagen. Furthermore, the levels of both cGMP and cAMP were also increased by the exogenous addition of LF to thrombin- and collagen-stimulated platelets. These results mean that LF increases cGMP directly and cAMP indirectly, and thus inhibits thrombin- or collagen-induced rat platelet aggregation. Both the thrombin time (TT) and activated partial thromboplastin time (APTT) were prolonged more in citrated platelet-poor plasma from COLF than in that from CO. The level of lipids such as triglyceride, total cholesterol, high density lipoprotein-cholesterol and low density lipoprotein-cholesterol was decreased in serum from COLF more than in that of CO. Thus, these results suggest that dietary LF regulates the levels of cGMP and cAMP, and prolongs the time interval (TT, APTT) between the conversion of fibrinogen to fibrin. Accordingly, our data demonstrate that dietary LF has an antithrombotic effect in vivo.

Administration of PG201 has therapeutic effects on CIA. Protection of cartilage was particularly prominent. PG201 is a potential therapy for rheumatoid arthritis.

Despite a multitude of reports on anti-inflammatory properties of ginseng extracts or individual ginsenosides, data on antiarthritic effect of ginseng saponin preparation with mixed ginsenosides is limited. On the other hand, a combined therapy of safe and inexpensive plant-derived natural products such as ginsenosides can be considered as an alternative to treat arthritis. Our previous in vitro data displayed a strong anti-inflammatory action of red ginseng saponin fraction-A (RGSF-A). We, herein, report a marked antiarthritic property of RGSF-A rich in ginsenoside Rb1, Rc, and Rb2. Collagen-induced arthritic (CIA) mice were treated with RGSF-A or methotrexate (MTX) for 5 weeks. Joint pathology, serum antibody production and leukocye activation, cytokine production in the circulation, lymph nodes, and joints were examined. RGSF-A markedly reduced severity of arthritis, cellular infiltration, and cartilage damage. It suppressed CD3+/CD69+, CD4+/CD25+, CD8+ T-cell, CD19+, B220/CD23+ B-cell, MHCII+/CD11c+, and Gr-1+/CD11b+ cell activations. It further suppressed anti-CII- or anti-RF-IgG/IgM, TNF-α, IL-1β, IL-17, and IL-6 secretions but stimulated IL-10 levels in the serum, joint, or splenocyte. RGSF-A attenuated arthritis severity, modified leukocyte activations, and restored cytokine imbalances, suggesting that it can be considered as an antiarthritic agent with the capacity to ameliorate the immune and inflammatory responses in CIA mice.

Red ginseng saponin fraction-A (RGSF-A) contains a high percentage of panaxadiol saponins that were isolated from Korean red ginseng by ultrafiltration. The aim of this study was to elucidate the effects of RGSF-A on the porcine distal left anterior descending (LAD) coronary artery. The relaxant responses to RGSF-A were examined during contractions induced by 100 nM U46619 (9,11-dideoxy-9a,11a-methanoepoxy-prostaglandin F2a), a stable analogue of thromboxane A2. RGSF-A dose-dependently induced biphasic (fast- and slow-) relaxation in the distal LAD coronary artery in the presence of an intact endothelium. The fast-relaxation was quickly achieved in a minute, and then the slow-relaxation was slowly developed and sustained for more than thirty minutes after the administration of RGSF-A. The slow-relaxation had a tendency to be bigger than the fast-relaxation. Fast relaxation induced by RGSF-A was almost blocked by Nω-Nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor. However slow-relaxation induced by RGSF-A was only partially inhibited by L-NAME and ODQ. In the endothelium-removed ring, RGSF-A evoked only slow-relaxation to a certain extent. These data suggest that RGSF-A induced both endothelium dependent fast- and slow-relaxation and endothelium independent slow-relaxation in the porcine distal LAD coronary artery. The endothelium dependent fast-relaxation is mediated by the nitric oxide (NO)-cGMP pathway, and the endothelium dependent slow-relaxation is at least partially mediated by the NO-cGMP pathway. However, the endothelium-independent slow-relaxation remains to be elucidated.

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Background and Objective: Patients with ischemic or hemorrhagic stroke require strict BP control to prevent hemorrhagic transformation or hematoma expansion. Acute elevations in BP are often treated with IV labetalol. Dedicated stroke units often have automated bedside monitoring of vital signs. Standard automated BP monitoring alerts practitioners to trends that lead to more steady control of BP rather than frequent acute interventions. We evaluated patients who were treated in a stroke unit after the institution of automated bedside monitoring. Comparison was made to the number of times the patients were dosed acutely using labetalol with a control group of patients who were not receiving automated bedside monitoring. The objective was to determine if there was a significant difference in care. Methods: Patients were evaluated over a 12-month period (2014) after the incorporation of bedside automated BP monitoring in a dedicated stroke unit at a university affiliated, comprehensive stroke center. The number of times each patient during this time frame received IV labetalol for acute elevations in BP was compared with a time period spanning 12-months prior (2013); there was no automated BP monitoring performed. The average interventions were compared with a t-test by using SPSS V22. Comparisons of patient population and type of pathology were matched appropriately. Results: Of the 1,326 patients who presented for ischemic or hemorrhagic strokes during the 24-month period evaluated, 25 required multiple injections of IV labetalol for acute BP control. Of these, 12 patients were on automated vital signs and BP monitoring, and 13 were not. The mean number of IV labetalol interventions implemented in the group being monitored was 2.8, while the mean number of treatments given to patients not being monitored was 5.9 (p=.016). Conclusion: In our study there is a trend towards better blood pressure control with adequate adjustment of oral medications for monitored patients in our dedicated stroke unit. Prevention of sudden elevations in BP may translate into lower rates of hemorrhagic transformation or hematoma expansion and confer better outcomes in stroke patients. Larger prospective studies are required to corroborate our findings.