Fig 1: IL-1ß-induced prostaglandin E2 release and COX-2 mRNA and protein levels in canine synovial fibroblasts. Cells treated with (closed circle) or without (open circle) canine recombinant IL-1ß (100 pM) showed an increase in prostaglandin E2 (PGE2) release (A) and COX-2 mRNA levels (C) in a time-dependent manner, but did not affect COX-1 mRNA levels (E). Cells were treated with the indicated concentrations of IL-1ß for 48 h (B) or 6 h (D) and assayed for PGE2 release (B) and COX-2 mRNA levels (D) in a dose-dependent manner. Cells treated with IL-1ß (100 pM) for 0–48 h showed increased protein levels of COX-2 in a time-dependent manner (F; first row), but did not affect the protein levels of COX-1 (F; second row). The expression of COX-2 (G) and COX-1 (H) in IL-1ß-stimulated cells were compared with the expression at 0 h. Results have been represented as mean ± standard error (SE) from biological triplicates. *P < 0.05. Cell lysates (10 µg protein) were used for immunoblotting. ß-actin was used as the internal standard (F; third row).
Fig 2: Effect of GTB on cyclooxygenase-1 (COX-1) protein expression in gastric mucosal tissue in rat detected by Western blotting. Rats were exposed to hypoxia (in hypobaric chamber, equal to the parameter in altitude 5000 m), hypoxia (H)+omeprazole treatment (7 mg/kg/d), and hypoxia (H)+GTBs-treatment (0.25, 0.5, and 1.0 mg/kg/d) for 6 days. GAPDH protein expression was used as a control. Relative expression levels of COX-1. Data are mean ± S.D. of three identical experiments. #P < 0.05 as compared with the control group; *P < 0.05 as compared with the hypoxia group.
Fig 3: Frataxin-deficient models have increased expression of COX2 and no alterations in COX1 or cPLA2 expression. (A and D) Cerebellum of KIKO has 4.40-fold increased expression of Cox2 while no changes in Cox1 and cPla2 or the active phosphorylated cPLA2 were observed compared with C57Bl/6 WT. (B) Cerebellum of YG8 hemizygote showed 1.35-fold increased Cox2 expression and no change in Cox1 expression was observed compared with YG8 homozygote. (C) Patient B-lymphocytes had 1.71-fold increased expression of COX2 expression with no changes in COX1 expression compared with healthy B-lymphocytes. The KIKO and YG8 samples were normalized to ß-tubulin and B-lymphocyte samples were normalized to ß-actin. Bars represent averages ± standard deviations (n = 4, P < 0.05*, P < 0.005**).
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