Saeed Hosseini

Publications (2)8.77 Total impact

• Article: Immune Dysfunction During Alcohol Consumption and Murine AIDS: The Protective Role of Dehydroepiandrosterone Sulfate

  Jeongmin Lee, Ramon T. Sepulveda, Shugang Jiang, Zhen Zhang, Paula Inserra, Yan Zhang, Saeed Hosseini, Ronald R. Watson
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  ABSTRACT: Acquired immune deficiency syndrome (AIDS) is a clinical disorder caused by the human immunodeficiency virus (HIV) after development of severe immunosuppressive changes. Chronic ethanol (EtOH) consumption accentuates the severity of murine AIDS (MAIDS). Because hormone production is often suppressed by chronic EtOH intake, as well as retrovirus infection, we investigated whether hormone supplementation during chronic EtOH consumption contributes to slowing immune dysfunction caused by LP-BMS infection and/or EtOH use. Because dehydroepiandrosterone sulfate (DHEAS) was previously shown to have immune-enhancing properties during MAIDS, we determined whether DHEAS reduced cytokine dysregulation otherwise exacerbated by chronic EtOH intake during MAIDS. Adult female C57BL/6 mice were infected with LP-BMS murine retrovirus. Some were fed 40% EtOH in drinking water and agar gel for 16 weeks postinfection. EtOH consumption further inhibited T- and B-cell proliferation beyond suppression due to retrovirus infection. Interleukin (1L)-2 release produced by concanavalin A-stimulated splenocytes was reduced by EtOH use by infected and uninfected mice. DHEAS overcame much of the ecffects induced by retrovirus infection and/or EtOH use. IL-4 secretion and IL-6 secretion were enhanced. Hepatic vitamin E levels were decreased by murine retrovirus infection, as well as by EtOH use in both uninfected and infected mice. In addition, DHEAS (0.01%) supplementation during MAIDS prevented the further dysrcgulation of cytokines and hepatic lipid peroxidation due to EtOH intake, partially restorcd T- and B-cell proliferation, and maintained hepatic vitamin E levels to near normal levels.
  Alcoholism Clinical and Experimental Research 05/2006; 23(5):856 - 862. · 3.34 Impact Factor
• Article: Solar ultraviolet-induced erythema in human skin and nuclear factor-kappa-B–dependent gene expression in keratinocytes are modulated by a French maritime pine bark extract

  Claude Saliou, Gerald Rimbach, Hadi Moini, Laura McLaughlin, Saeed Hosseini, Jeongmin Lee, Ronald R Watson, Lester Packer
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  ABSTRACT: The procyanidin-rich French maritime pine bark extract Pycnogenol (PBE) has been investigated for its effect in protecting human skin against solar UV-simulated light-induced erythema. Twenty-one volunteers were given an oral supplementation of Pycnogenol: 1.10 mg/kg body weight (b. wt.)/d for the first 4 weeks and 1.66 mg/kg b. wt./d for the next 4 weeks. The minimal erythema dose (MED) was measured twice before supplementation (baseline MED), once after the first 4 weeks of supplementation, and a last time at the end of the study. The UVR dose necessary to achieve 1 MED was significantly increased during PBE supplementation. Since the activation of the pro-inflammatory and redox-regulated transcription factor NF-κB is thought to play a major role in UVR-induced erythema, the effect of PBE was also investigated in the human keratinocyte cell line HaCaT. PBE, added to the cell culture medium, inhibited UVR-induced NF-κB–dependent gene expression in a concentration-dependent manner. However, NF-κB–DNA-binding activity was not prevented, suggesting that PBE affects the transactivation capacity of NF-κB. These data indicate that oral supplementation of PBE reduces erythema in the skin. Inhibition of NF-κB–dependent gene expression by PBE possibly contributes to the observed increase in MED.
  Free Radical Biology and Medicine 02/2001; · 5.42 Impact Factor