rabbit polyclonal antibody against ho-1  (Huabio Inc)

Journal: PLOS Neglected Tropical Diseases

Article Title: Iron-overload-induced ferroptosis in mouse cerebral toxoplasmosis promotes brain injury and could be inhibited by Deferiprone

doi: 10.1371/journal.pntd.0011607

Figure Lengend Snippet: (A) Electrophoretic map of the hippocampal DNA of uninfected and infected mice. (B) RNA-seq data-based differentially expressed gene analysis between uninfected and infected mice hippocampus. Data of n = 3 biological replicates. (C) GO analyses of RNA-seq data showed the top 20 enriched GO terms pre- and post-infection. (D) KEGG analyses of RNA-seq data showed the top 20 enriched pathways in the hippocampus between pre- and post-infection. (E) Representative H&E images of hippocampal formation CA1 from uninfected and infected mice. Single black arrowheads, necrotic cells. (F) Western blot analysis of GFAP, IFN-γ, TNF-α, TGF-β and Arg-1 expression in hippocampus. * P <0.05, ** P <0.01, *** P <0.001. Mice were infected with TgCtwh3 for seven days.

Article Snippet: Rabbit polyclonal antibodies against GFAP, TGF-β, ARG1, TNF-α (1:1000, Affinity Bioscience, USA), IFN-γ, NRF2, COX2 (1:500, Wanleibio, China), TfR1, Fpn, NCOA4, SLC7A11, GPx4 (1:1000, Abmart, China), HO-1 (1:1000, HUABIO, China), rabbit monoclonal antibody against FTH1 (1:1000, HUABIO, China), and mouse monoclonal antibody against 4-Hydroxynonenal (1:1000, 4-HNE, R&D Systems, United States) were incubated with the PVDF membranes overnight at 4°C.

Techniques: Infection, RNA Sequencing, Western Blot, Expressing

Journal: PLOS Neglected Tropical Diseases

Article Title: Iron-overload-induced ferroptosis in mouse cerebral toxoplasmosis promotes brain injury and could be inhibited by Deferiprone

doi: 10.1371/journal.pntd.0011607

Figure Lengend Snippet: (A) Representative H&E images of the hippocampal formation of CA1 from mice in the con + vehicle, con + DFP, TgCtwh3 + vehicle, and TgCtwh3 + DFP groups. Single black arrowheads, necrotic cells. (B) Western blot analysis of GFAP, IFN-γ, TNF-α, TGF-β and Arg-1 expression in hippocampus. (C) Morris water maze trajectory diagram of mice arriving at the platform on the fifth day of place navigation and the spatial probe test. (D) Escape latency of the place navigation. (E) Platform crossover number of the spatial probe. (F) Swimming speed of the spatial probe. (G) Body weight changes of mice in the above four groups. (H) Percent survival of mice in the above four groups, n = 10 mine. (I) QRT-PCR was used to detect the mRNA expression level of Tg SAG1 in hippocampus of TgCtwh3 infected mice, and GAPDH was used as reference mRNA, and statistical significance was calculated by two-tailed Student’s t-test, n = 6 mice. Data represent mean ± SD of n = 7 biological replicates. Statistical significance was calculated by Brown-Forsythe and Welch’s ANOVA with Dunnett’s T3 multiple comparison test. # P <0.05, ## P <0.01, ### P <0.001, #### P <0.0001 versus control; * P <0.05, ** P <0.01, *** P <0.001; ns, not significant. Mice were infected with TgCtwh3 for seven days.

Article Snippet: Rabbit polyclonal antibodies against GFAP, TGF-β, ARG1, TNF-α (1:1000, Affinity Bioscience, USA), IFN-γ, NRF2, COX2 (1:500, Wanleibio, China), TfR1, Fpn, NCOA4, SLC7A11, GPx4 (1:1000, Abmart, China), HO-1 (1:1000, HUABIO, China), rabbit monoclonal antibody against FTH1 (1:1000, HUABIO, China), and mouse monoclonal antibody against 4-Hydroxynonenal (1:1000, 4-HNE, R&D Systems, United States) were incubated with the PVDF membranes overnight at 4°C.

Techniques: Western Blot, Expressing, Quantitative RT-PCR, Infection, Two Tailed Test, Comparison, Control

Journal: PLoS ONE

Article Title: Sulforaphane Protects Rodent Retinas against Ischemia-Reperfusion Injury through the Activation of the Nrf2/HO-1 Antioxidant Pathway

doi: 10.1371/journal.pone.0114186

Figure Lengend Snippet: HO-1 expression in the retina was determined by immunofluorescent staining. (A-D, E-H) Representative micrographs of retinal sections obtained at 24 h (A-D) or 7 days (E-H) after ischemia and stained using an anti-HO-1 antibody. (I, J) Quantification of HO-1 immunofluorescent intensity (arbitrary units) at 24 h (I) or 7 days (J) after I/R injury. (K, L) Representative immunoblot showing the HO-1 protein levels in the whole retina (upper panel) at 24 h (K) or 7 days (L) after ischemia and densitometric analysis of HO-1 expression relative to the loading control (lower panel) (mean ± SEM, n = 5). Control: sham-operated animal, I/R: vehicle-treated animal with 1 h of ischemia, and SF+I/R: SF-pretreated animal with 1 h of ischemia. * p<0.05, ** p<0.01, *** p<0.001 compared with control, # p<0.05, ### p<0.001 compared with I/R within the same time point, one-way ANOVA with Bonferroni post hoc test. The conventions are the same as in .

Article Snippet: After blocking with 5% BSA for 1 hour at room temperature, the membranes were incubated with primary antibodies at 4°C overnight, including goat polyclonal antibody against ChAT (Millipore Corp, Billerica, MA), rabbit polyclonal antibody against HO-1 (Stressgen Biotech Inc., Philadelphia, PA.), and rabbit polyclonal anti–β-actin (Sigma-Aldrich Corp).

Techniques: Expressing, Staining, Western Blot

Journal: PLoS ONE

Article Title: Sulforaphane Protects Rodent Retinas against Ischemia-Reperfusion Injury through the Activation of the Nrf2/HO-1 Antioxidant Pathway

doi: 10.1371/journal.pone.0114186

Figure Lengend Snippet: The involvement of HO-1 in the protective effects of SF on the retina after I/R was determined using a specific HO-1 inhibitor, ZnPP. (A) Representative immunoblot of the HO-1 protein levels in the whole retina (upper panel) at 24 h after ischemia and densitometric analysis of HO-1 expression relative to the loading control (lower panel). (B) Micrographs of retinal sections obtained 24 h after ischemia and RGCs stained with Rbpms. (C) Quantitative analysis of the Rbpms-positive cells in the GCL (mean ± SEM, n = 5). (D) Micrographs of retinal sections obtained 24 h after ischemia and stained with an amacrine cell-specific marker, anti-ChAT. (E) Quantitative analysis of ChAT-positive cells in GCL and the INL (mean ± SEM, n = 5). Control: sham-operated animal, I/R: vehicle-treated animal with 1 h of ischemia, SF+I/R: SF-pretreated animal with 1 h of ischemia, and SF+ZnPP+I/R: SF-pretreated animal with ZnPP injection 24 h before 1 h of ischemia. + p<0.05, ++ p<0.01 compared with control, * p<0.05, *** p<0.001 compared with I/R, # p<0.05, ## p<0.01 compared with SF+I/R, one-way ANOVA with Bonferroni post hoc test. The conventions are the same as in .

Article Snippet: After blocking with 5% BSA for 1 hour at room temperature, the membranes were incubated with primary antibodies at 4°C overnight, including goat polyclonal antibody against ChAT (Millipore Corp, Billerica, MA), rabbit polyclonal antibody against HO-1 (Stressgen Biotech Inc., Philadelphia, PA.), and rabbit polyclonal anti–β-actin (Sigma-Aldrich Corp).

Techniques: Western Blot, Expressing, Staining, Marker, Injection