Fig 1: Individual values of (A) myeloperoxidase concentration (pg/mL) and (B) MPO activity (mU/mL) in the cerebrospinal fluid in male and female patients with idiopathic Parkinson’s disease and controls. Mean and standard deviation are represented with solid lines (black lines, cohort of patients and control participants; men are represented in blue and women in orange). * p < 0.01. Abbrev.: CSF, cerebrospinal fluid; MPO, myeloperoxidase.
Fig 2: Effect of β-Lap on pancreatic MPO activity and inflammatory changes during caerulein-induced AP. (A) Pancreatic MPO activity. (B,C) Pancreatic mRNA levels of MCP-1, NLRP3, and ASC measured using qRT-PCR. (D,E) Total pancreatic homogenates were obtained from each experimental group and pancreatic protein levels of NLRP3 and ASC were measured by ELISA, and blotted with anti-caspase-1. (F) Serum IL-1β levels analysed by ELISA. Each value represents the mean ± SD (n = 5). *P < 0.05, **P < 0.01.
Fig 3: MPO activity enhances mitoxantrone-induced TOP2-DNA covalent complex formation and H2AX phosphorylation. (A and B) NB4 cells were pretreated with 200 μM SA for 48 hours followed by a 1-hour incubation with 0.5 or 1 μM mitoxantrone, or a vehicle control. TOP2-DNA covalent complexes and γH2AX were quantified as in Figs. 1 and 3. Data are expressed relative to the mean values obtained with 1 μM mitoxantrone in the absence of SA. (C) Quantification of MPO activity in K562MPO line 2 compared with NB4 and parental K562 cells. (D) MPO expression in K562 cells results in enhanced mitoxantrone-induced TOP2-DNA protein complex formation. Data are expressed relative to the mean value obtained for parental K562 cells treated with 1 μM mitoxantrone. Numbers of replicates are indicated. *P < 0.05; **P < 0.01; ***P < 0.001.
Fig 4: MPO activity results in raised levels of etoposide-induced H2AX phosphorylation. (A) NB4 cells were pretreated for 48 hours with SA (200 µM) then incubated with etoposide (10 or 100 µM). (B) K562 and K562MPO cell lines were incubated with 10 and 100 µM etoposide or dimethyl sulfoxide vehicle control. For both (A) and (B), γH2AX was quantified by immunofluorescence. Analysis was carried out as described for TARDIS analysis in Fig. 1. Data are expressed relative to the mean values obtained with 100 μM etoposide in the absence of SA (A) or in wild-type parental K562 cells (B). Numbers of replicates are indicated. *P < 0.05; **P < 0.01; ***P < 0.001.
Fig 5: ATRA enhances macrophage phagocytosis in ALI rats. (A) MPO activity of alveolar macrophages was measured. (B) Phagocytic rate and (C) phagocytic index of macrophages were detected using the chicken erythrocyte phagocytosis method. (D) MFI value of macrophages and (E) the percentage of phagocytic positive cells were detected using flow cytometry. The cell experiments were repeated three times independently. Data are expressed as mean ± standard deviation and analyzed using one-way analysis of variance, followed by Tukey's multiple comparisons test. **P<0.01 vs. control group; ##P<0.01 vs. ALI group. ATRA, all-trans retinoic acid; ALI, acute lung injury; MPO, myeloperoxidase; MFI, mean fluorescence intensity.
Supplier Page from Abcam for Myeloperoxidase (MPO) Activity Assay Kit (Colorimetric)