The Effect of Hydrocortisone Induced Deficiency Syndrome on Tumor Growth in H22 Liver Cancer Mice

OBJECTIVE To study the effect of hydrocortisone induced deficiency syndrome on tumor growth in H22 liver cancer mice. METHODS Kunming male mice were randomly divided into normal control group， tumor model group，hydrocortisone group， and hydrocortisone tumor group. Mice were given hydrocortisone for 14 d， and H22 liver cancer cells were inoculated simultaneously under the axilla to replicate the liver cancer mice model on the first day of hydrocortisone administration. The mice body mass and tumor size were observed. The mice were executed， and the spleen and thymus were weighed and the organic index were calculated. Then， mRNA expression of adrenal steroid synthase genes and tumor growth associated genes were detected by qPCR. Akt and p-Akt protein expression were assayed by Western blot. RESULTS Compared with normal control group， the spleen of tumor model group increased significantly (P<0.05). The gene expression of Cyp11a1，Cyp11b1 and Cyp11b2 significantly reduced (P<0.05). The spleen and thymus of the two hydrocortisone groups significantly decreased (P<0.01)， and Star， Cyp11a1， Cyp21a1 and Cyp11b1 of adrenal all down-regulated (P<0.05). Compared with the tumor model group， tumor tissue of hydrocortisone tumor mice was smaller in 7th day (P<0.05). At the same time， the hydrocortisone inhibited Akt1 expression in tumor tissue (P<0.05)， prompted Foxo3 expression (P<0.05)， inhibited Akt and p-Akt protein expression. Compared with the hydrocortisone group， the atrophy of spleen and thymus alleviated and adrenal steroid synthase genes all up-regulated (P<0.05) in the hydrocortisone tumor groups. CONCLUSION Hydrocortisone can induce the deficiency syndrome in mice by inhibiting the endocrine immune function， the proliferation of tumor reduce in early stage， while tumor growth going up in persistent deficiency syndrome mice.