tag:blogger.com,1999:blog-11335328.post5221022335435331919..comments2023-10-22T11:35:26.366+02:00Comments on GOLEM Blog: Una prueba necesariaÁngel M. Felicísimohttp://www.blogger.com/profile/08908536576379820142noreply@blogger.comBlogger1125tag:blogger.com,1999:blog-11335328.post-64876205364838357522007-09-17T23:55:00.000+02:002007-09-17T23:55:00.000+02:00Un par de ejemplos:Phytother Res. 2002 Sep;16(6):5...Un par de ejemplos:<BR/><BR/>Phytother Res. 2002 Sep;16(6):550-4. Screening of selected plant extracts for in vitro inhibitory activity on human<BR/>immunodeficiency virus. Bedoya LM, Palomino SS, Abad MJ, Bermejo P, Alcami J.<BR/><BR/>As part of our screening of anti-AIDS agents from natural sources, extracts of 15<BR/>medicinal plants widely used in the folk medicines of North America and Europe<BR/>were evaluated in vitro. Most of the extracts tested were relatively nontoxic to <BR/>human lymphocytic MT-2 cells, but only the extracts of Hysopp officinalis and<BR/>Dittrichia viscosa exhibited anti-HIV activity in an in vitro MTT assay. The 50% <BR/>hydroalcohol extract of Hysopp officinalis and the aqueous extract of Dittrichia <BR/>viscosa showed inhibitory effects against HIV-1 induced infections in MT-2 cells <BR/>at concentrations ranging from 50 to 100 microg/mL and 25 to 400 microg/mL,<BR/>respectively. Both extracts showed no appreciable cytotoxicity at these<BR/>concentrations. <BR/><BR/>AIDS. 2005 Dec 2;19(18):2087-95. Indirubin-3'-monoxime, a derivative of a Chinese antileukemia medicine, inhibits <BR/>P-TEFb function and HIV-1 replication. Heredia A, Davis C, Bamba D, Le N, Gwarzo MY, Sadowska M, Gallo RC, Redfield RR.<BR/><BR/>OBJECTIVE: To evaluate the effects of the cyclin dependent kinase (CDK) inhibitor<BR/>Indirubin-3'-monoxime (IM) on Tat-mediated transactivation function, a step of<BR/>the HIV-1 cycle that is not currently targeted in antiviral therapy. METHODS: The<BR/>effects of IM on CDK implicated in HIV-1 Tat transactivation function were<BR/>evaluated by kinase assays, transfection experiments, RNase protection assay and <BR/>RT-PCR analysis of viral transcripts. The antiviral effect of IM was investigated<BR/>in cells from HIV-1 infected individuals as well as in cell lines, primary<BR/>lymphocytes and monocyte-derived macrophages. The antiviral activity of IM was<BR/>also tested against drug-resistant HIV-1. RESULTS: IM inhibits the kinase<BR/>activity of CDK9 [50% inhibitory concentration (IC50) of 0.05 microM], the<BR/>catalytic subunit of Positive transcription elongation factor b (P-TEFb).<BR/>Inhibition of CDK9 activity by IM results in abrogation of Tat-induced expression<BR/>of HIV-1 RNA in cell lines. In addition, IM inhibits the replication of HIV-1 in <BR/>both peripheral blood mononuclear cells (IC50 of 1 microM) and macrophages (IC50 <BR/>of 0.5 microM). IM is effective against primary and drug-resistant strains of<BR/>HIV-1. Importantly, the antiviral effects of the drug were seen at concentrations<BR/>that did not affect cell proliferation. CONCLUSIONS: Non-toxic concentrations of <BR/>IM inhibit HIV-1 by blocking viral gene expression mediated by the cellular<BR/>factor P-TEFb. The drug is effective against wild-type and drug-resistant strains<BR/>of HIV-1. IM may help control replication of HIV-1 in patients by disrupting a<BR/>step of the HIV-1 cycle that is not being targeted in current antiretroviral<BR/>treatments.Antonio Mashttps://www.blogger.com/profile/02456945924633753263noreply@blogger.com