The amount of ferulic acid in the AS was 0 61 mgg Results Conce

The amount of ferulic acid in the AS was 0. 61 mgg. Results Concentration and time effects of Angelica Sinensis on the viability of myotubes The viability of cells in the group without AS treatment was expressed as 100%. As shown in Table 1, at 24 h, the cell viability of myotubes decreased by 9%, 16%, and 26% when exposed to 104, 105, and 106 ngmL of AS, re spectively, inhibitor purchase compared with Inhibitors,Modulators,Libraries the cells in the untreated con trol group. At 48 h, the cell viability of the myotubes decreased by 9%, 25%, and 31% when exposed to 104, 105, and 106 ngmL of AS, respectively, compared with the cells in the untreated control group. At 72 h, the cell viability of the myotubes decreased by 9%, 25%, and 32% when exposed to 104, 105, and 106 ngmL of AS, respect ively, compared with the cells in the untreated control group.

The cell viability at concentrations of 105 and 106 ngmL of AS was significantly decreased compared with the control group after the same period of culturing. The Inhibitors,Modulators,Libraries results indicated that AS was not harmful to myotubes at concentrations of 1, 10, or 102 ngmL. Inhibitors,Modulators,Libraries Therefore, an AS concentration of 10 ngmL was used to induce hypertrophy in the experiment. Inhibitors,Modulators,Libraries Myotube hypertrophy induced by Angelica Sinensis To determine whether AS is functionally critical for myotube hypertrophy, the influence of AS on myotube thickness was examined. After 72 h of incu bation, highly thickened myotubes were observed in the AS treated group. The myotube diameter of 2 groups exhibited normal distribution. The result indicated that the average myotube diameter in the AS group increased 1. 34 0.

13 fold compared with the NON group. This clearly revealed that AS induced myotube hypertrophy. Involvement of the PI3KAktmTOR pathway Inhibitors,Modulators,Libraries in Angelica Sinensis induced myotube hypertrophy To examine the role of the PI3KAktmTOR signaling pathway in AS induced myotube hypertrophy, pharma cologic experiments were conducted using inhibitors that interfered with this pathway. IGF 1 stimulation that activated the pathway was used as a positive control. The PI3K inhibitor, wortmannin, reduced the diameters of AS treated myotubes by 25%, and the diameters of the positive controls by approxi mately 30%. The mTOR inhibitor, rapamycin, behaved similarly to wortmannin Second, further investigation showed that Akt phosphoryl ation induced by 15 min of AS treatment was significantly reduced beyond the non AS supplements level, using wortmannin.

essentially the same results were obtained in the samples regarding Akt phosphoryl ation induced by 45 min of AS treatment. These data suggested that AS promoted Akt phosphoryl ation through the PI3K pathway, which was observed in the case of IGF Vorinostat HDAC3 1 stimulation. Mamallian target of rapamycin phosphorylation induced by Angelica Sinensis The procedure for this experiment resembled the afore mentioned time course analysis.

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