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Abstract. Ginsenoside Rb3 is one of the major active components in protopanaxdiol type ginsenosides, and has demonstrated anti-diabetic activity. However, the mechanism of this action has yet to be elucidated. The present study investigated the effects of ginsenoside Rb3 on the AMP-activated protein kinase (AMPK) gluconeogenesis pathway. The present study involved the use of HepG2 cells and western blot analysis to systematically evaluate the effect of ginsenoside Rb3 on AMPK signaling proteins and key factors of gluconeogenesis [phosphoenolpyruvate carboxykinase (PEPCK), glucose-6-phosphatase, forkhead transcription factor 1 (FOXO1) and hepatic nuclear receptor 4α (HNF4α)]. The results indicated that 25 µM ginsenoside Rb3 significantly activated AMPK activity, increased the ratio of p-AMPK/total-AMPK, and had synergistic effects with the activator of AICAR on the activation of AMPK. Further analysis indicated that the expression of the transcription factor FOXO1 and HNF4α protein, two important factors in the pathway of HepG2 cell gluconeogenesis, was significantly suppressed by ginsenoside Rb3. PEPCK and G6Pase were subsequently inhibited, which led to the suppression of gluconeogenesis. These effects were partially blocked by the AMPK inhibitor, Compound C, which indicated that the inhibition effects of ginsenoside Rb3 on hepatic gluconeogenesis were predominantly due to the activation of the AMPK signaling pathway. These data suggested that ginsenoside Rb3 can suppress hepatic gluconeogenesis, at least partially through stimulation of AMPK activity.

The present study aimed to investigate the effect of combined treatment with quercetin and Adriamycin (doxorubicin) on the development of refractory acute leukemia. Primary leukemic cells were isolated from patients with refractory drug-resistant acute leukemia. The Cell Counting Kit-8 assay was used to detect the proliferation of cells treated with a range of doses of Adriamycin, quercetin and a combination of the two drugs. Non-irradiated mice were used to establish a T cell acute lymphoblastic leukemia (T-ALL) model, which was subsequently treated with Adriamycin, quercetin and a combination of the two drugs. The survival time was recorded, and white and red blood cells and platelets in mouse peripheral blood were counted. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) content of cardiac tissues were measured as indicators of oxidative stress and damage. Proliferation of primary leukemic cells was reduced by Adriamycin depending on the dose (0.06, 0.6 or 6 µg/ml) and treatment duration (24, 48 or 72 h) compared with the vehicle treated group. Co-treatment with quercetin achieved a similar suppression of leukemic cell proliferation when a lower dose of Adriamycin (0.03, 0.3 or 3 µg/ml) was administered for the same duration. The survival of non-irradiated mice with T-ALL was improved by co-treatment with a high dose of Adriamycin and quercetin compared with either treatment alone. Compared with treatment with Adriamycin alone, the combined treatment with Adriamycin and quercetin significantly enhanced the SOD activity and reduced the MDA content in the heart. Therefore, quercetin may enhance the effects of Adriamycin on refractory acute leukemia.

The effect of similar atom substitution on the glass forming ability (GFA) of Al86Ni9(Y, Sm)5 (x = (0, 1, 1.5, 2, 3, 4, 5)) metallic glasses (MGs) was explored on the basis of the theory of the Fermi sphere-Brillouin zone interaction. Similar atom substitution (Sm) mainly affects the static structure between Al atoms and Y (Sm) atoms, changing the diameter of the pseudo-Brillouin zone (KP). Its effect on the Fermi level and Brillouin zone size is characterized with spectroscopy experiments. The |δ|=|KP – 2KF| criterion is used to evaluate the effect of the Sm element substitution on the GFA. This criterion can help us obtain the optimal GFA composition (Al86Ni9Y3.5Sm1.5) of Al86Ni9(Y, Sm)5 amorphous alloys, confirmed also by the experimental results.