SOD3 Antibody - #DF7753

Fig. 1 SOD3 is a host factor associated with host vulnerability to parasite infection. a Progressively increased expression of SOD3 was observed during P. y. yoelii YM infection. The mouse illustration was created with http://BioRender.com (publishing license: CZ26UIGFUP). b Serum SOD3 expression was elevated in mice after infection with P. berghei ANKA, with peaks observed after 5 days and 9 days. Five biological replicates were included in the analysis; healthy controls were three biological replicates. Statistical significance tested by one-way ANOVA, and multiple comparisons to each day were corrected using Dunnet’s method. WT mice of average survival time was 9 days from the time of challenge. c SOD3 in the sera of P. falciparum–infected patients from the China-Myanmar border (endemic areas, n = 20), other endemic areas (cases were travel-related, n = 24) and healthy donors (endemic and nonendemic areas, n = 41) as measured by enzyme-linked immunosorbent assay (ELISA). SOD3 levels were significantly elevated in malaria patients from all areas compared with corresponding healthy donors. Two-tailed student’s t test was used to test for significant differences between two groups. d SOD3−/− mice (n = 20) showed significant extended survival time than the WT littermates (n = 20) after P. y. yoelii YM infection. Survived mice in SOD3−/− group were humanely euthanized accordingly to the Institutional Animal Care and Use Committee-approved criteria. e Knockout of SOD3 extended the survival of P. y. yoelii 17XL-infected mice, n = 10. The survived mice in SOD3−/− group were humanely euthanized accordingly to approved criteria. f Knockout of SOD3 decreased parasitemia in both seven and eight days after T. b. brucei infection. Two-tailed student’s t test was used to test for significant differences between two groups. g Knockout of SOD3 extended the survival of T. gondii-infected mice. The survived mice in SOD3−/− group were humanely euthanized accordingly to approved criteria. Kaplan‒Meier survival curves were calculated using the survival time for each mouse in all groups, and significance was determined by the log-rank test. For d-f, n indicates mouse numbers in graphs. Histograms present the mean ± SD. Source data are provided as a Source Data file.

FIGURE 4. BNTA regulated Redox-related gene expression and inhibited intracellular ROS generation. (A) Representative fluorescence images of RANKL-stimulated ROS production in BMMs with or without pre-treatment of indicated dose of BNTA. (B) Quantification of the number of ROS positive cells per field (n = 3 per group). All data are presented as mean ± SD. *p < 0.05, **p < 0.01. (C) qPCR analysis of mRNA expression of SOD1, SOD2, and SOD3 relative to GAPDH in BMMs stimulated by RANKL for 5 days without stimulation of BNTA (n = 3 per group). All data are presented as mean ± SD. ****p < 0.0001 compared with control group. (D–F) qPCR analysis of redox-related genes expression of SOD1, SOD2, and SOD3 relative to GAPDH in BMMs stimulated by RANKL for 5 days with or without an indicated dose of BNTA (n = 3 per group). All data are presented as mean ± SD. *p < 0.05, ***p < 0.001, ****p < 0.0001 compared with control group. (G) Representative immunofluorescence staining images of decalcified bone sections for protein expression of SOD1, SOD2, and SOD3. (H–J) Quantitative analysis of protein expression of SOD1, SOD2, and SOD3 in vivo. *p < 0.05, **p < 0.01 compared with control group.

Figure 6. Expression of SOD3 and COL2A1 in human bone mar-row-derived mesenchymal stem cells overexpressing long non-coding RNA (LncRNA) MEG3 after cultured in osteogenic medi-um for 14 days.