دورية أكاديمية
Structural requirements of taxoids for nitric oxide and tumor necrosis factor production by murine macrophages.
العنوان: | Structural requirements of taxoids for nitric oxide and tumor necrosis factor production by murine macrophages. |
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المؤلفون: | Kirikae T; Department of Microbiology, Jichi Medical School, Tochigi-ken, Japan. tkirikae@jichi.ac.jp, Ojima I, Kirikae F, Ma Z, Kuduk SD, Slater JC, Takeuchi CS, Bounaud PY, Nakano M |
المصدر: | Biochemical and biophysical research communications [Biochem Biophys Res Commun] 1996 Oct 03; Vol. 227 (1), pp. 227-35. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
اللغة: | English |
بيانات الدورية: | Publisher: Elsevier Country of Publication: United States NLM ID: 0372516 Publication Model: Print Cited Medium: Print ISSN: 0006-291X (Print) Linking ISSN: 0006291X NLM ISO Abbreviation: Biochem Biophys Res Commun Subsets: MEDLINE |
أسماء مطبوعة: | Publication: <2002- >: San Diego, CA : Elsevier Original Publication: New York, Academic Press. |
مواضيع طبية MeSH: | Macrophages, Peritoneal/*drug effects , Nitric Oxide/*biosynthesis , Paclitaxel/*pharmacology , Tumor Necrosis Factor-alpha/*biosynthesis, Animals ; Cell Line ; Female ; Macrophage Activation/drug effects ; Macrophages, Peritoneal/metabolism ; Mice ; Mice, Inbred C3H |
مستخلص: | Taxol (paclitaxel), a microtubule stabilizer with antitumor activity, mimics the actions of lipopolysaccharide (LPS) on murine macrophages (M phi). In the present study, a variety of synthetic analogs of paclitaxel were examined for their potencies to induce nitric oxide (NO) and tumor necrosis factor (TNF) production by peritoneal M phi from LPS-responsive C3H/HeN, and LPS-hyporesponsive C3H/HeJ mice, and by M phi-like LPS-responsive J774.1 and its mutant LPS-hyporesponsive J7.DEF3 cells. In this structure-activity relationship study, we found that (i) the benzoyl group at the C-3' position of paclitaxel is the most important site to activate C3H/HeN M phi; (ii) the phenyl group at C-3' is not a requisite for the activity; (iii) there is good correlation between NO and TNF production by the M phi in response to compounds, except for the analogs having a tert-butoxycarbonyl (10-acetyldocetaxel) or a thiophene-2-carbonyl group at C-3'-N instead of a benzoyl group, which is more dominant in TNF than in NO production; (iv) the compounds tested induce neither NO nor TNF production by C3H/HeJ M phi; (v) active compounds to C3H/He M phi induce TNF production by J7.DEF3 cells as well as J774.1 cells; and (vi) there is no correlation between the NO/TNF inducibility to C3H/HeN M phi and growth inhibitory activity against M phi-like J774.1 and J7.DEF3 cells. These data also suggest that the binding of taxoid/LPS to tubulin is not essential for the M phi activation. |
معلومات مُعتمدة: | GM 427980 United States GM NIGMS NIH HHS |
المشرفين على المادة: | 0 (Tumor Necrosis Factor-alpha) 31C4KY9ESH (Nitric Oxide) P88XT4IS4D (Paclitaxel) |
تواريخ الأحداث: | Date Created: 19961003 Date Completed: 19961125 Latest Revision: 20151119 |
رمز التحديث: | 20240627 |
DOI: | 10.1006/bbrc.1996.1494 |
PMID: | 8858130 |
قاعدة البيانات: | MEDLINE |
تدمد: | 0006-291X |
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DOI: | 10.1006/bbrc.1996.1494 |