Low molecular weight lignin suppresses activation of NF-κB and HIV-1 promoter

Human immunodeficiency virus type 1 (HIV-1) is a cytopathic retrovirus and the primary etiological agent of acquired immunodeficiency syndrome (AIDS) and related disorders. In cells chronically infected with HIV-1, nuclear factor-κB (NF-κB) activation by external stimuli such as tumor necrosis factor α (TNFα) augments replication of HIV-1. NF-κB involves in many diseases such as inflammation, cancer, and Crohn’s disease. In this paper, we exhibit that (i) HIV-1gene expression was inhibited by lignin, (ii) fraction of small molecular mass in HBS lignin (less than 0.5 kDa) had stronger inhibitory effects than large molecular mass (more than 1.3 kDa), (iii) lignin also inhibited activation of NF-κB induced by TNFα, (iv) among six lignin dimer-like compounds, compound 6 containing β-5 bond has more potent inhibitory activity than compounds 1, 2, 3, 4 and 5, which contain β-1, β-O-4, 5-5, or β–β structural units. These results suggested that small molecules of lignin inhibit HIV-1 replication through suppression of HIV-1 transcription from LTR including activation via NF-κB. Low molecular lignin may be a beneficial material or drug leads as a new class for AIDS and NF-κB-related diseases.

Low molecular weight lignin (less than 0.5 kDa) suppresses activation of NF-κB induced by TNF-α and HIV-1 gene expression. Among six lignin dimer-like compounds, compound 6 containing β-5 bond has more potent inhibitory activity than compounds 1, 2, 3, 4, and 5, which contain β-1, β-O-4, 5-5, and β–β structural units. These results suggested that the small molecule of lignin inhibits HIV-1 replication through suppression of HIV-1 transcription from LTR via NF-κB activation.Figure optionsDownload as PowerPoint slide