Effect of astragaloside on mRNA expression of PI3K/Akt/mTOR signal transduction in anemia model mice induced by chemotherapy

To study the influence of astragaloside on mRNA expression of PI3K/Akt/mTOR signal transduction in anemia model mice induced by chemotherapy, 48 male BALB/c mice which were 6-7 week old were picked as the research objects and randomly divided into four groups, blank group, model group, astragaloside group and astragaloside IV group. Each group was 12 mice. Chemotherapy anemia model was established by cyclophosphamide. The mice were drawn blood from eyeball after 14 days treatment. The QPCR was used to test the mRNA concentrations of Akt, PI3K, BCL-xl, bad, FoxO, mTOR, PTEN in mouse spleen. In comparison of blank group, astragaloside group and astragaloside IV group,the erythrocyte counting and values of Hb in model group were significantly lower (P<0.05). The volumes mRNA of Akt,PI3K,BCL-xl,bad,mTOR were lower in blank group, compared with other groups (P<0.05 or P<0.01). The similar trend in astragaloside IV group except PI3K, comparing with blank group (P<0.05 or P<0.01). The contents of these five genes were no significant differentiations between astragaloside group and blank group. The statistics were obvious between astragaloside group and astragaloside IV group (P<0.05 or P<0.01). The concentrations of FoxO, PTEN were higher in model group,compared with blank group and astragaloside group (P<0.05 or P<0.01), but no difference with astragaloside IV group. Comparing with blank group, the volumes of these two genes were increased in astragaloside IV group (P<0.05), FoxO was higher in astragaloside group (P<0.05), but PTEN was not significant. There was no the same as astragaloside group and Astragaloside IV group. Therefore, astragaloside could increase the contents of Akt, PI3K, BCL-xl, bad, mTOR (P<0.01), decrease the concentrations of FoxO, PTEN (P<0.05). The changes in cyclophosphamide-induced anemia were highly significant by astragaloside. It could be related to the mRNA expression of PI3K/Akt/mTOR Signal Transduction.