Fig 1: N-AS-acetylated COX2 produces SPMs.a Human recombinant COX2 treated in the presence or absence of 500 µM N-AS or aspirin was incubated with AA, EPA, or DHA in presence of human 5-LOX, and then SPM precursors were identified using systematic LC-MS/MS. Representative chromatogram showing the SPM precursors (Top, 15-HETE; Middle, 18-HEPE; Bottom, 17-HDHA). b Human recombinant COX2 treated in the presence of 500 µM N-AS or aspirin was incubated with AA, EPA, or DHA in presence of human 5-LOX. Related MS/MS spectra employed for identification of SPMs. 15R-LXA4, RvE1, and RvD1. c Quantification of 15R-LXA4, RvE1, and RvD1 in COX2 WT and COX2 S565A treated with 5-LOX in presence of N-AS, aspirin or not (n = 5–7 independent experiments per group). c One-way analysis of variance, Tukey’s post hoc test. All error bars indicate s.e.m. Source data are provided as a Source data file.
Fig 2: Carvacrol modulates the activity of cancer targets in a FaDu, K562, and A549 cell lines. Treated cancer cell lines were determined by the protocol described in materials and methods section. (A) Suppression of ornithine decarboxylase (ODC) activity by carvacrol. (B) Destruction of cyclooxygenase-2 (COX-2) activity by carvacrol. (C) Inflection of lipoxygenase 5 (LOX-5) activity by carvacrol. (D) Modulatory effect of carvacrol on hyaluronidase (HYAL) activity. (E) The suppression of cathepsin D (CATD) activity by carvacrol. The graph is shown in percentage inhibition. Data are presented as mean ± SD (n = 3). Comparatively, carvacrol exhibits a pronounced effect against ODC in FaDu cells.
Supplier Page from Cayman Chemical for 5-Lipoxygenase (human, recombinant)
EC Number: 1.13.11.34