Most of the compounds have physiologically active properties, and their biological properties are often attributed to the heteroatoms contained in their molecules, and most of these heteroatoms also appear in cyclic structures. A Journal, Article, Research Support, Non-U.S. Gov’t, Research Support, U.S. Gov’t, Non-P.H.S., Journal of Investigative Dermatology called Pentoxifylline, pentifylline, and interferons decrease type I and III procollagen mRNA levels in dermal fibroblasts: Evidence for mediation by nuclear factor 1 down-regulation, Author is Duncan, Matthew R.; Hasan, Anthony; Berman, Brian, which mentions a compound: 1028-33-7, SMILESS is CN1C=NC(N(C(N2CCCCCC)=O)C)=C1C2=O, Molecular C13H20N4O2, Electric Literature of C13H20N4O2.
Pentoxifylline (PTX) is a methylxanthine that exhibits multiple biol. activities, including the inhibition of collagen synthesis by dermal fibroblasts. Because some PTX activities have recently been linked to transcription factor-mediated regulation of gene transcription, we have investigated if PTX acts to inhibit collagen synthesis at a transcriptional locus by measuring procollagen mRNA levels and by assaying for the presence of an activator of procollagen gene promoters, nuclear factor (NF)-1. The effects of another methylxanthine, pentifylline (PTF), shown herein to be a ten-fold more potent inhibitor of collagen synthesis than PTX, and interferon-α, -β, and -γ were studied in parallel. Anal. of extracellular protein and RNA from 48-h-treated fibroblasts showed that PTX, PTF, and interferons decreased α1(I), α2(I), and α1(III) procollagens by reducing the steady-state levels of the corresponding procollagen mRNA transcripts. Reduction of procollagen mRNA levels appeared to be dependent on new protein synthesis, as it was prevented by treatment with cycloheximide. Assay for the presence of nuclear NF-1 by gel mobility shift anal. showed that extracts from interferon, PTX, and PTF-treated fibroblasts lacked proteins recognizing the consensus DNA binding sequence for NF-1. Taken together, these observations suggest interferons and methylxanthines may inhibit fibroblast collagen synthesis by a common mechanism requiring new protein synthesis that suppresses procollagen gene transcription through down-regulation of NF-1.
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Reference:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem