a(CHEBI:"desferrioxamine B")
DFX also reduced the MAC content in the clot at day-3 (33.0 ± 6.6 vs. 56.2 ± 9.2 ng/g in the vehicle-treated group, p<0.05, Fig. 5B). PubMed:27125525
The present study found that DFX treatment reduces MAC formation in the clot. PubMed:27125525
Heme-induced necroptosis is reversed by deferoxamine, a Fe chelator. PubMed:24904418
Treatment with Hx or DFO diminished the increase of some M1 polarization markers in BMDMs following treatment with hemolytic RBCs (supplemental Figure 14). PubMed:26675351
We found that hemoglobin contents in hematoma were significantly higher in the DFX treated group compare to the vehicle-treated group (15.9 ± 1.8 vs. 11.8 ± 0.8 mg/g, p<0.05, Fig. 5A). PubMed:27125525
DFX treatment also caused a significant reduction in infiltrating CD163-positive and HO-1 positive cell in the hematoma at day 3 (Figs. 6A and B) and day 7 (Suppl Figures II & III). PubMed:27125525
The loss of CD47 in the clot was reduced significantly by DFX treatment at day 3 (CD47/GAPDH: 1.32 ± 0.16 in ICH+DFX group vs. 0.74 ± 0.07 in ICH + vehicle group, p<0.05, Fig. 5C) and day 7 (p<0.01, Suppl Figure I). PubMed:27125525
DFX also reduced CD47 loss and microglia/macrophage infiltration after ICH suggesting it also affects erythrophagocytosis. PubMed:27125525
DFX treatment also caused a significant reduction in infiltrating CD163-positive and HO-1 positive cell in the hematoma at day 3 (Figs. 6A and B) and day 7 (Suppl Figures II & III). PubMed:27125525
Western blot analysis showed that the protein expression of HO-1 was decreased in the hematoma in the DFX treated group at day 3( HO-1/GAPDH: 0.32 ± 0.04 vs. 0.98 ± 0.07 in the vehicle-treated group, p<0.05, Fig. 6B) and day 7 (p<0.05, Suppl Figure III). PubMed:27125525
There was a tendency that lysed RBC-induced brain edema was less in deferoxamine-treated group (brain water content in the ipsilateral hemisphere: 79.8±0.6% vs. 80.5±0.7% in the saline coinjection group, n¼6, P40.05). PubMed:24667910
In combination, these finding may underlie our previous results showing that DFX slows hematoma resolution after ICH in aged rats 12. PubMed:27125525
Coinjection of deferoxamine with lysed RBC reduced ventricular enlargement (47.8±17.8 vs. 59.9±15.7mm3 in saline coinjection group, Po0.05, Figure 6). PubMed:24667910
The major findings of this study are (1) intraventricular injection of lysed RBCs but not packed RBCs resulted in hydrocephalus; (2) lysed RBCs upregulated brain HO-1 and ferritin levels; (3) intraventricular injection of iron also caused hydrocephalus; and (4) iron chelation with deferoxamine reduced lysed RBC-induced hydrocephalus. PubMed:24667910
DFX also reduced CD47 loss and microglia/macrophage infiltration after ICH suggesting it also affects erythrophagocytosis. PubMed:27125525
DFX treatment also caused a significant reduction in infiltrating CD163-positive and HO-1 positive cell in the hematoma at day 3 (Figs. 6A and B) and day 7 (Suppl Figures II & III). PubMed:27125525
DFX treatment also caused a significant reduction in infiltrating CD163-positive and HO-1 positive cell in the hematoma at day 3 (Figs. 6A and B) and day 7 (Suppl Figures II & III). PubMed:27125525
Coinjection of deferoxamine with lysed RBC reduced ventricular enlargement (47.8±17.8 vs. 59.9±15.7mm3 in saline coinjection group, Po0.05, Figure 6). PubMed:24667910
The major findings of this study are (1) intraventricular injection of lysed RBCs but not packed RBCs resulted in hydrocephalus; (2) lysed RBCs upregulated brain HO-1 and ferritin levels; (3) intraventricular injection of iron also caused hydrocephalus; and (4) iron chelation with deferoxamine reduced lysed RBC-induced hydrocephalus. PubMed:24667910
There was a tendency that lysed RBC-induced brain edema was less in deferoxamine-treated group (brain water content in the ipsilateral hemisphere: 79.8±0.6% vs. 80.5±0.7% in the saline coinjection group, n¼6, P40.05). PubMed:24667910
Heme-induced necroptosis is reversed by deferoxamine, a Fe chelator. PubMed:24904418
Treatment with Hx or DFO diminished the increase of some M1 polarization markers in BMDMs following treatment with hemolytic RBCs (supplemental Figure 14). PubMed:26675351
We found that hemoglobin contents in hematoma were significantly higher in the DFX treated group compare to the vehicle-treated group (15.9 ± 1.8 vs. 11.8 ± 0.8 mg/g, p<0.05, Fig. 5A). PubMed:27125525
DFX also reduced the MAC content in the clot at day-3 (33.0 ± 6.6 vs. 56.2 ± 9.2 ng/g in the vehicle-treated group, p<0.05, Fig. 5B). PubMed:27125525
The present study found that DFX treatment reduces MAC formation in the clot. PubMed:27125525
These results suggested that the treatment of DFX reduced the process of hemolysis after ICH, which might be due to alleviating MAC formation. PubMed:27125525
The loss of CD47 in the clot was reduced significantly by DFX treatment at day 3 (CD47/GAPDH: 1.32 ± 0.16 in ICH+DFX group vs. 0.74 ± 0.07 in ICH + vehicle group, p<0.05, Fig. 5C) and day 7 (p<0.01, Suppl Figure I). PubMed:27125525
Western blot analysis showed that the protein expression of HO-1 was decreased in the hematoma in the DFX treated group at day 3( HO-1/GAPDH: 0.32 ± 0.04 vs. 0.98 ± 0.07 in the vehicle-treated group, p<0.05, Fig. 6B) and day 7 (p<0.05, Suppl Figure III). PubMed:27125525
In combination, these finding may underlie our previous results showing that DFX slows hematoma resolution after ICH in aged rats 12. PubMed:27125525
Chelation of growth-medium iron with deferoxamine (DFO, 10 μM) led to a reduction in bacterial growth, as compared with non-chelated controls (Fig. 2a). PubMed:27798618
Expectedly, and in line with previous report (13), treatment of macrophages with DFO abolished ferroportin and ferritin induction by heme, whereas TfR1 expression was lowered upon heme and combined treatment with heme and DFO (Fig. 7D). PubMed:29212341
Expectedly, and in line with previous report (13), treatment of macrophages with DFO abolished ferroportin and ferritin induction by heme, whereas TfR1 expression was lowered upon heme and combined treatment with heme and DFO (Fig. 7D). PubMed:29212341
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.