@entity701 has a protective effect on @entity205 -induced XXXX .

@entity137 @entity870 @entity205 @entity842 @entity701 @entity460 @entity35 @entity1370 @entity1865
@entity205 ( @entity870 ) is an immunosuppressive drug which induces severe adverse effects such as @entity1370 and nephrotoxicity. In several therapeutic protocols @entity870 is used in association with corticosteroids to obtain better therapeutic results. Recently, our studies showed that @entity870 increases blood pressure while inhibit @entity842 (NO) production in vivo. In this study we evaluated in @entity35 cardiomyocytes the effects of @entity870 , used alone or in association with @entity701 (HY), on intracellular @entity460 concentration, NO production and lipid peroxidation ( @entity1865 level). Our results demonstrated that @entity870 increased intracellular @entity460 and such effect was dose-dependent. HY used alone, slightly decreased intracellular @entity460 , while dramatically reduced @entity870 -induced @entity460 fluxes. @entity870 (3.2 microM) increased lipid peroxidation and this effect was blunted by HY. Both @entity870 and HY inhibited NO production in @entity35 cardiomyocytes acting on this pathway synergically. Our results demonstrated that in @entity35 cardiomyocytes, @entity870 @entity137 is due to a @entity460 overload, which in turn induce lipid peroxidation and determines oxidative stress-induced cell injury. Treatment with HY effectively inhibits @entity870 -induced @entity137 , decreasing lipid peroxidation as well as @entity460 intracellular concentration. Our findings seem to suggest that glucocorticoids may be effective in reducing @entity870 -induced @entity1370 at concentrations which are consistent with current therapeutic doses.
