Linked Life Data

16539678

Source:http://linkedlifedata.com/resource/pubmed/id/16539678

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pubmed-article:16539678pubmed:abstractTextImpaired inflammatory functions may be critical factors in the mechanisms of severe CNS disorders classified as the human immunodeficiency virus-1 (HIV-1)-associated dementia (HAD). Evidence indicates that a viral gene product, the transactivator of transcription protein (Tat), can markedly contribute to these events. We herein report that sulfated polymannuroguluronate (SPMG), a novel anti-acquired immunodeficiency syndrome drug candidate now in a phase II clinical trial, significantly reversed Tat-induced release of pro-inflammatory cytokines [tumour necrosis factor (TNF)-alpha, interleukin (IL)-1beta) and IL-6] and dose dependently decreased the accumulation of reactive oxygen species and nitric oxide in THP-1 cells. Furthermore, SPMG potently arrested Tat-triggered protein kinase C (PKC)-dependent PKC-mu activation, and blocked the downstream extracellular-signal regulated kinase 1/2- and c-jun amino-terminal kinase-mediated signalling pathways. These molecular mechanisms could be attributed to the fact that SPMG preferentially bound to the basic domain (amino acids 47-57) of the Tat protein with high affinity (K(D) approximately 8.69 x 10(-10) m), leading to abrogation of Tat-mediated neuroinflammation and neurotoxicity. These data demonstrate that SPMG might serve as a valuable therapeutic intervention for Tat-induced profound pro-inflammatory effects in the brain, and subsequent pathologic events of HAD.lld:pubmed
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pubmed-article:16539678pubmed:articleTitleSulfated polymannuroguluronate, a novel anti-acquired immune deficiency syndrome drug candidate, blocks neuroinflammatory signalling by targeting the transactivator of transcription (Tat) protein.lld:pubmed
pubmed-article:16539678pubmed:affiliationDepartment of Pharmacology, Marine Drug and Food Institute, Ocean University of China, Qingdao.lld:pubmed
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