期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 226, 期 12, 页码 3385-3391出版社
WILEY-BLACKWELL
DOI: 10.1002/jcp.22691
关键词
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资金
- National Natural Sciences Foundation of China [30800580]
- Beijing Nova Program [2007B014]
- Beijing Natural Science Foundation [5093025, 5112004]
- National Basic Research Program of China [2009CB930200]
Chromatin remodeling, especially in relation to the transactivator Tat, is an essential event for human immunodeficiency virus-1 (HIV-1) transcription. Curcumin has been shown to suppress pathways linked to HIV-1 replication. We investigated whether curcumin had the potential to inhibit Tat-induced long terminal repeat region (LTR) transactivation. As we shown, curcumin inhibited Tat-induced LTR transcativation, while knockdown of histone deacetylase 1 (HDAC1) by siRNA potentiated Tat-induced HIV-1 transcativation. Curcumin reversed Tat-induced down-regulation of HDAC1 expression in multinuclear activation of galactosidase indicator (MAGI) cells. Treatment with curcumin reversed Tat-induced dissociation of HDAC1 from LTR; and curcumin caused a decline in the binding of p65/NF kappa B to LTR promoters stimulated by Tat. Curcumin attenuated Tat-induced p65 phosphorylation and IKK phosphorylation. Curcumin reversed Tat-mediated reduction in AMPK activation and downstream acetyl-CoA carboxylase (ACC) activation. Collectively, our data provide new insights into understanding of the molecular mechanisms of curcumin inhibited Tat-regulated transcription, suggesting that targeting AMPK/HDAC1/NF kappa B pathway could serve as new anti-HIV-1 agents. J. Cell. Physiol. 226: 3385-3391, 2011. (C) 2011 Wiley Periodicals, Inc.
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