Dehydroepiandrosterone Sulfate Inhibited Immune Dysfunction Induced by LP-BM5 Leukemia Retrovirus Infection through Regulating Thl/Th2 Type Cytokine mRNA Expression and Oxidative Stress in Murine AIDS Model

摘要

LP-BM5 murine leukemia retrovirus induces the excessive oxidative stress and immune dysfunction leading to B cell leukemia and murine AIDS with cytokine dysfunction. In the present study, the immune restoratory effect of antioxidant hormone dedydroepiandrosterone sulfate (DHEAS) was investigated in the primary splenocytes from LP-BM5 retrovirus-infected C57BL/6 mice. DHEAS significantly increased T and B cell response to mitogen and normalized the unbalanced production of Thl/Th2 type cytokines. In particular, both protein and mRNA expression of IL-4, IL-6, and TNF-a were down-regulated by DHEAS treatment, whereas IL-2 and IFN~ 7 level were increased. This result suggests that DHEAS directly or indirectly regulates the gene expression of Thl/Th2 type cytokines in transcription level. In addition, DHEAS treatment decreased the hepatic lipid peroxidation and preserved vitamin E level in liver cells. These results suggested that DHEAS could effectively prevent immune dysfunction by regulating cytokinesecretion and preventing the oxidative stress in murine AIDS.