Flavonoid Baicalin Inhibits HIV-1 Infection at the Level of Viral Entry

Flavonoid Baicalin Inhibits HIV-1 Infection at the Level of Viral Entry

Baicalin (BA) is a flavonoid compound purified from medicinal plant Scutellaria baicalensis Georgi and has been shown to possess anti-inflammatory and anti-HIV-1 activities. In an effort to elucidate the mechanism of the anti-inflammatory effect of BA, we recently found that this flavonoid compound...

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Bibliographic Details
Published in:Biochemical and biophysical research communications Vol. 276; no. 2; pp. 534 - 538
Main Authors: Li, Bao Qun, Fu, Tao, Dongyan, Yao, Mikovits, Judy A., Ruscetti, Francis W., Wang, Ji Ming
Format: Journal Article
Language:English
Published: United States Elsevier Inc 24-09-2000
Subjects:
Antiviral Agents - pharmacology
Baicalin
CCR5 protein
CD4 Antigens - metabolism
CXCR4 protein
flavonoid
flavonoids
Flavonoids - pharmacology
fusion
HIV Envelope Protein gp120 - metabolism
HIV Envelope Protein gp120 - physiology
HIV-1
HIV-1 - drug effects
HIV-1 - physiology
Human immunodeficiency virus 1
Humans
Scutellaria baicalensis
Tumor Cells, Cultured
viral entry
HIV-1
fusion
viral entry
flavonoid
baicalin
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Summary:Baicalin (BA) is a flavonoid compound purified from medicinal plant Scutellaria baicalensis Georgi and has been shown to possess anti-inflammatory and anti-HIV-1 activities. In an effort to elucidate the mechanism of the anti-inflammatory effect of BA, we recently found that this flavonoid compound was able to form complexes with selected chemokines and attenuated their capacity to bind and activate receptors on the cell surface. These observations prompted us to investigate whether BA could inhibit HIV-1 infection by interfering with viral entry, a process known to involve interaction between HIV-1 envelope proteins and the cellular CD4 and chemokine receptors. We found that BA at the noncytotoxic concentrations, inhibited both T cell tropic (X4) and monocyte tropic (R5) HIV-1 Env protein mediated fusion with cells expressing CD4/CXCR4 or CD4/CCR5. Furthermore, presence of BA at the initial stage of HIV-1 viral adsorption blocked the replication of HIV-1 early strong stop DNA in cells. Since BA did not inhibit binding of HIV-1 gp120 to CD4, we propose that BA may interfere with the interaction of HIV-1 Env with chemokine coreceptors and block HIV-1 entry of target cells. Therefore, BA can be used as a basis for developing novel anti-HIV-1 agents.
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ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.2000.3485