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rabbit polyclonal anti cd36 antibody (Novus Biologicals)

Name: rabbit polyclonal anti cd36 antibody
Brand: Novus Biologicals
Rating: 90 (6 reviews)

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Novus Biologicals rabbit polyclonal anti cd36 antibody

High expression of <t>CD36</t> in the kidney of rats fed with high-fat diet and in podocytes treated with PA. (a) Immunofluorescence staining of CD36 and nephrin in renal tissue derived from control subjects or high-fat diet rats (×400). NC: the normal control group that was given basic feed for 10 weeks, HFD: the high-fat diet group that was provided a high-fat diet for 10 weeks. (b) and (c) Quantification of the fluorescence intensity of CD36 and nephrin staining ( n = 5, * P < 0.05 vs NC group). (d) The western blot of CD36 expression in the kidney of rats. NC: the normal control group that was given basic feed for 4 weeks, HFD4W: the group that was fed a high-fat diet for 4 weeks, HFD10W: the group that was fed a high-fat diet for 10 weeks. (e) Densitometric analysis of CD36 ( n = 3, * P < 0.05 vs NC group). (f) The western blot of CD36 expression in the podocytes. Podocytes were incubated with different concentrations of PA (0–300 µmol/L) for 12 h; CD36 expression was measured by western blot analysis (53, 78, and 88 kDa). β-actin was used as an internal control. Representative images are shown. (g) Densitometric analysis of CD36 ( n = 3, * P < 0.05 vs 0 μmol/L, # P < 0.05 vs 50 μmol/L, & P < 0.05 vs μmol/L).

Rabbit Polyclonal Anti Cd36 Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit polyclonal anti cd36 antibody/product/Novus Biologicals
Average 90 stars, based on 6 article reviews

rabbit polyclonal anti cd36 antibody - by Bioz Stars, 2026-03

90/100 stars

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1) Product Images from "CD36-mediated podocyte lipotoxicity promotes foot process effacement"

Article Title: CD36-mediated podocyte lipotoxicity promotes foot process effacement

Journal: Open Medicine

doi: 10.1515/med-2024-0918

High expression of CD36 in the kidney of rats fed with high-fat diet and in podocytes treated with PA. (a) Immunofluorescence staining of CD36 and nephrin in renal tissue derived from control subjects or high-fat diet rats (×400). NC: the normal control group that was given basic feed for 10 weeks, HFD: the high-fat diet group that was provided a high-fat diet for 10 weeks. (b) and (c) Quantification of the fluorescence intensity of CD36 and nephrin staining ( n = 5, * P < 0.05 vs NC group). (d) The western blot of CD36 expression in the kidney of rats. NC: the normal control group that was given basic feed for 4 weeks, HFD4W: the group that was fed a high-fat diet for 4 weeks, HFD10W: the group that was fed a high-fat diet for 10 weeks. (e) Densitometric analysis of CD36 ( n = 3, * P < 0.05 vs NC group). (f) The western blot of CD36 expression in the podocytes. Podocytes were incubated with different concentrations of PA (0–300 µmol/L) for 12 h; CD36 expression was measured by western blot analysis (53, 78, and 88 kDa). β-actin was used as an internal control. Representative images are shown. (g) Densitometric analysis of CD36 ( n = 3, * P < 0.05 vs 0 μmol/L, # P < 0.05 vs 50 μmol/L, & P < 0.05 vs μmol/L).

Figure Legend Snippet: High expression of CD36 in the kidney of rats fed with high-fat diet and in podocytes treated with PA. (a) Immunofluorescence staining of CD36 and nephrin in renal tissue derived from control subjects or high-fat diet rats (×400). NC: the normal control group that was given basic feed for 10 weeks, HFD: the high-fat diet group that was provided a high-fat diet for 10 weeks. (b) and (c) Quantification of the fluorescence intensity of CD36 and nephrin staining ( n = 5, * P < 0.05 vs NC group). (d) The western blot of CD36 expression in the kidney of rats. NC: the normal control group that was given basic feed for 4 weeks, HFD4W: the group that was fed a high-fat diet for 4 weeks, HFD10W: the group that was fed a high-fat diet for 10 weeks. (e) Densitometric analysis of CD36 ( n = 3, * P < 0.05 vs NC group). (f) The western blot of CD36 expression in the podocytes. Podocytes were incubated with different concentrations of PA (0–300 µmol/L) for 12 h; CD36 expression was measured by western blot analysis (53, 78, and 88 kDa). β-actin was used as an internal control. Representative images are shown. (g) Densitometric analysis of CD36 ( n = 3, * P < 0.05 vs 0 μmol/L, # P < 0.05 vs 50 μmol/L, & P < 0.05 vs μmol/L).

Techniques Used: Expressing, Immunofluorescence, Staining, Derivative Assay, Control, Fluorescence, Western Blot, Incubation

CD36 mediated lipid uptake under PA induction. (a) Lipid accumulation in control subjects or high-fat diet rats are stained with Oil Red O (×400). (b) Representative immunofluorescence images of podocytes stained with BODIPY (×300). Ctr: control group, in which podocytes were treated with 1% BSA. PA: PA group, in which podocytes were treated with 150 µmol/L PA for 12 h. PA + DMSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with DMSO for 4 h. PA + SSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with 50 µmol/L SSO for 4 h.

Figure Legend Snippet: CD36 mediated lipid uptake under PA induction. (a) Lipid accumulation in control subjects or high-fat diet rats are stained with Oil Red O (×400). (b) Representative immunofluorescence images of podocytes stained with BODIPY (×300). Ctr: control group, in which podocytes were treated with 1% BSA. PA: PA group, in which podocytes were treated with 150 µmol/L PA for 12 h. PA + DMSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with DMSO for 4 h. PA + SSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with 50 µmol/L SSO for 4 h.

Techniques Used: Control, Staining, Immunofluorescence

Oxidative stress participated in CD36-mediated podocyte FP effacement induced by PA. (a) The images and fluorescence intensity of intracellular ROS stained by the fluorescent probe DCFH-DA. * P < 0.05 vs Ctr group, # P < 0.05 vs PA group, Δ P < 0.05 vs PA + DMSO group. (b) Podocytes were treated with 150 µmol/L PA for 12 h with or without NAC or SSO pretreatment, and podocytes were stained with Alexa Fluor 568-labeled phalloidin. Ctr: control group, in which podocytes were treated with 1% BSA. PA: PA group, in which podocytes were treated with 150 µmol/L PA for 12 h. PA + DMSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with DMSO for 4 h. PA + SSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with 50 µmol/L SSO for 4 h.

Figure Legend Snippet: Oxidative stress participated in CD36-mediated podocyte FP effacement induced by PA. (a) The images and fluorescence intensity of intracellular ROS stained by the fluorescent probe DCFH-DA. * P < 0.05 vs Ctr group, # P < 0.05 vs PA group, Δ P < 0.05 vs PA + DMSO group. (b) Podocytes were treated with 150 µmol/L PA for 12 h with or without NAC or SSO pretreatment, and podocytes were stained with Alexa Fluor 568-labeled phalloidin. Ctr: control group, in which podocytes were treated with 1% BSA. PA: PA group, in which podocytes were treated with 150 µmol/L PA for 12 h. PA + DMSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with DMSO for 4 h. PA + SSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with 50 µmol/L SSO for 4 h.

Techniques Used: Fluorescence, Staining, Labeling, Control

Hypothetical mechanism for PA-induced podocyte FP effacement. PA exposure upregulates CD36 expression and then induces an abnormal accumulation of lipids, further promoting oxidative stress. Excessive ROS generation activates actin reorganization and ultimately results in podocyte FP effacement, which may occur through TRPC6 channel-activated dysregulation of intracellular Ca 2+ in podocytes.

Figure Legend Snippet: Hypothetical mechanism for PA-induced podocyte FP effacement. PA exposure upregulates CD36 expression and then induces an abnormal accumulation of lipids, further promoting oxidative stress. Excessive ROS generation activates actin reorganization and ultimately results in podocyte FP effacement, which may occur through TRPC6 channel-activated dysregulation of intracellular Ca 2+ in podocytes.

Techniques Used: Expressing

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Journal: Open Medicine

Article Title: CD36-mediated podocyte lipotoxicity promotes foot process effacement

doi: 10.1515/med-2024-0918

Figure Lengend Snippet: High expression of CD36 in the kidney of rats fed with high-fat diet and in podocytes treated with PA. (a) Immunofluorescence staining of CD36 and nephrin in renal tissue derived from control subjects or high-fat diet rats (×400). NC: the normal control group that was given basic feed for 10 weeks, HFD: the high-fat diet group that was provided a high-fat diet for 10 weeks. (b) and (c) Quantification of the fluorescence intensity of CD36 and nephrin staining ( n = 5, * P < 0.05 vs NC group). (d) The western blot of CD36 expression in the kidney of rats. NC: the normal control group that was given basic feed for 4 weeks, HFD4W: the group that was fed a high-fat diet for 4 weeks, HFD10W: the group that was fed a high-fat diet for 10 weeks. (e) Densitometric analysis of CD36 ( n = 3, * P < 0.05 vs NC group). (f) The western blot of CD36 expression in the podocytes. Podocytes were incubated with different concentrations of PA (0–300 µmol/L) for 12 h; CD36 expression was measured by western blot analysis (53, 78, and 88 kDa). β-actin was used as an internal control. Representative images are shown. (g) Densitometric analysis of CD36 ( n = 3, * P < 0.05 vs 0 μmol/L, # P < 0.05 vs 50 μmol/L, & P < 0.05 vs μmol/L).

Article Snippet: Briefly, after deparaffinization, rehydration, antigen recovery, and blocking, the sections were incubated with rabbit polyclonal anti-CD36 antibody (1:200; Novus Biologicals) and mouse monoclonal anti-nephrin antibody (1:200; Santa) overnight at 4°C.

Techniques: Expressing, Immunofluorescence, Staining, Derivative Assay, Control, Fluorescence, Western Blot, Incubation

Journal: Open Medicine

Article Title: CD36-mediated podocyte lipotoxicity promotes foot process effacement

doi: 10.1515/med-2024-0918

Figure Lengend Snippet: CD36 mediated lipid uptake under PA induction. (a) Lipid accumulation in control subjects or high-fat diet rats are stained with Oil Red O (×400). (b) Representative immunofluorescence images of podocytes stained with BODIPY (×300). Ctr: control group, in which podocytes were treated with 1% BSA. PA: PA group, in which podocytes were treated with 150 µmol/L PA for 12 h. PA + DMSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with DMSO for 4 h. PA + SSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with 50 µmol/L SSO for 4 h.

Techniques: Control, Staining, Immunofluorescence

Journal: Open Medicine

Article Title: CD36-mediated podocyte lipotoxicity promotes foot process effacement

doi: 10.1515/med-2024-0918

Figure Lengend Snippet: Oxidative stress participated in CD36-mediated podocyte FP effacement induced by PA. (a) The images and fluorescence intensity of intracellular ROS stained by the fluorescent probe DCFH-DA. * P < 0.05 vs Ctr group, # P < 0.05 vs PA group, Δ P < 0.05 vs PA + DMSO group. (b) Podocytes were treated with 150 µmol/L PA for 12 h with or without NAC or SSO pretreatment, and podocytes were stained with Alexa Fluor 568-labeled phalloidin. Ctr: control group, in which podocytes were treated with 1% BSA. PA: PA group, in which podocytes were treated with 150 µmol/L PA for 12 h. PA + DMSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with DMSO for 4 h. PA + SSO: podocytes were treated with 150 µmol/L PA for 12 h after being pretreated with 50 µmol/L SSO for 4 h.

Techniques: Fluorescence, Staining, Labeling, Control

Journal: Open Medicine

Article Title: CD36-mediated podocyte lipotoxicity promotes foot process effacement

doi: 10.1515/med-2024-0918

Figure Lengend Snippet: Hypothetical mechanism for PA-induced podocyte FP effacement. PA exposure upregulates CD36 expression and then induces an abnormal accumulation of lipids, further promoting oxidative stress. Excessive ROS generation activates actin reorganization and ultimately results in podocyte FP effacement, which may occur through TRPC6 channel-activated dysregulation of intracellular Ca 2+ in podocytes.

Techniques: Expressing

(A, B) Quantification of total cholesterol levels in multiple WT and RBP4-deficient cell types (A) and in serum from WT and RBP4-deficient mice (B). (C) Heatmap representation of RNA sequencing analysis showing differentially expressed genes related to cholesterol metabolism in WT and RBP4-deficient BMDMs. (D, E) qPCR analysis of CD36 mRNA expression in WT and RBP4-deficient BMDMs (D, left) and HEK293T cells (D, right), or in lung tissues from WT and RBP4-deficient mice (E). (F, G) Immunoblotting analysis of CD36 protein levels in multiple WT and RBP4-decficent cells as indicated (F) or in lung tissues from WT and RBP4-deficient mice (G). (H to J) Immunoblotting analysis of protein levels of CD36, total JNK, phosphorylated (p)-JNK, STAT1, and p-STAT1 as indicated in PK-15 or 3D4/21 cells pretreated with SP600125 (SP, 10 μM) or Resatorvid (TAK, 1 μM) for 2 hours, followed by treatment with rpRBP4 for 24 hours. (K) Immunoblotting analysis of protein expression of CD36, NP and M1 in PK-15 cells treated as described in (H), followed by infection with IAV WSN strain (MOI = 0.1) for 24 hours. (L) Immunoblotting analysis of CD36, p-STAT1, total STAT1 and RBP4 protein levels in HEK293T cells transfected with RBP4 expression plasmid or control empty vector, followed by treatment with Ruxolitinib (Ruxo, 5 μM) for 2 hours. (M) Immunoblotting analysis of CD36, p-STAT1, STAT1, STRA6 and RBP4 protein levels in HEK293T cells co-transfected with RBP4 expression plasmid and siRNA for STRA6 or negative control for 36 hours. (N) Immunoblotting analysis of CD36, p-JAK2, JAK2, p-STAT1, STAT1 and RBP4 protein levels in HEK293T cells transfected with RBP4 expression plasmid or control empty vector, followed by treatment with Ruxo (5 μM) for 2 hours or transfected with siRNA for STRA6 or negative control for 36 hours. Data are pooled from three independent experiments (A, B, D, E, mean ± SD) or representative of two independent experiments (F-N). * p < 0.05, ** p < 0.01 (Student’s t -tes t ).

Journal: PLOS Pathogens

Article Title: Retinol binding protein 4 enhances cellular cholesterol uptake to facilitate influenza A virus infection

doi: 10.1371/journal.ppat.1013623

Figure Lengend Snippet: (A, B) Quantification of total cholesterol levels in multiple WT and RBP4-deficient cell types (A) and in serum from WT and RBP4-deficient mice (B). (C) Heatmap representation of RNA sequencing analysis showing differentially expressed genes related to cholesterol metabolism in WT and RBP4-deficient BMDMs. (D, E) qPCR analysis of CD36 mRNA expression in WT and RBP4-deficient BMDMs (D, left) and HEK293T cells (D, right), or in lung tissues from WT and RBP4-deficient mice (E). (F, G) Immunoblotting analysis of CD36 protein levels in multiple WT and RBP4-decficent cells as indicated (F) or in lung tissues from WT and RBP4-deficient mice (G). (H to J) Immunoblotting analysis of protein levels of CD36, total JNK, phosphorylated (p)-JNK, STAT1, and p-STAT1 as indicated in PK-15 or 3D4/21 cells pretreated with SP600125 (SP, 10 μM) or Resatorvid (TAK, 1 μM) for 2 hours, followed by treatment with rpRBP4 for 24 hours. (K) Immunoblotting analysis of protein expression of CD36, NP and M1 in PK-15 cells treated as described in (H), followed by infection with IAV WSN strain (MOI = 0.1) for 24 hours. (L) Immunoblotting analysis of CD36, p-STAT1, total STAT1 and RBP4 protein levels in HEK293T cells transfected with RBP4 expression plasmid or control empty vector, followed by treatment with Ruxolitinib (Ruxo, 5 μM) for 2 hours. (M) Immunoblotting analysis of CD36, p-STAT1, STAT1, STRA6 and RBP4 protein levels in HEK293T cells co-transfected with RBP4 expression plasmid and siRNA for STRA6 or negative control for 36 hours. (N) Immunoblotting analysis of CD36, p-JAK2, JAK2, p-STAT1, STAT1 and RBP4 protein levels in HEK293T cells transfected with RBP4 expression plasmid or control empty vector, followed by treatment with Ruxo (5 μM) for 2 hours or transfected with siRNA for STRA6 or negative control for 36 hours. Data are pooled from three independent experiments (A, B, D, E, mean ± SD) or representative of two independent experiments (F-N). * p < 0.05, ** p < 0.01 (Student’s t -tes t ).

Article Snippet: The primary antibodies used in this study were sourced from commercial suppliers as follows: Rabbit polyclonal antibodies against RBP4 (1 : 2,000, 11774–1-AP), CD36 (1 : 2,000, 18836–1-AP), STRA6 (1 : 3,000, 22001–1-AP), p65 (1 : 1,000, 10745–1-AP) and β-actin (1 : 20,000, 66009–1-lg) were purchased from Proteintech Group Inc. Rabbit polyclonal antibodies against CD36 (1 : 1,000, CY5796) and FLAG (1 : 10,000, AB0030) were purchased from Abways.

Techniques: RNA Sequencing, Expressing, Western Blot, Infection, Transfection, Plasmid Preparation, Control, Negative Control

(A to D) Confocal microscopy (A and B) or flow cytometry (C and D) analysis of cholesterol uptake by Dil-OxLDL in WT and RBP4-deficient HEK293T cells or BMDMs. Scale bars, 100 μm. Statistics of mean fluorescence intensity was calculated by Image J software (A and B, right) or Flow Jo software (C and D, right). (E, F) Flow cytometry analysis of cholesterol uptake by Dil-OxLDL in WT, RBP4-deficient and CD36 overexpressing RBP4-deficient HEK293T cells (E) and BMDMs (F). Mean fluorescence intensities were quantified with Flow Jo software. (G, H) Flow cytometry analysis of SA expression in HEK293T cells (G, upper) transfected with hCD36 plasmid or in stable CD36-overexpressing iBMDMs (H, upper). Cells were left untreated or incubated with cholesterol for 1 hour at 37°C, followed by staining with SNA or MAL. Mean fluorescence intensities were quantified by Flow Jo software (lower panels). (I) Confocal microscopy analysis of SA expression and distribution in WT and CD36-overexpressing iBMDMs. Cells were left untreated or incubated with cholesterol for 1 hour at 37°C, followed by staining with SNA or MAL (green). Cell membranes were stained with Dil dye (red), and nuclei were counterstained with DAPI (blue). Data are representative (A-F, left, G, H, upper and I) or pooled from at least three independent experiments (A-F, right, G and H, lower, mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001 (Student’s t -test).

Journal: PLOS Pathogens

Article Title: Retinol binding protein 4 enhances cellular cholesterol uptake to facilitate influenza A virus infection

doi: 10.1371/journal.ppat.1013623

Figure Lengend Snippet: (A to D) Confocal microscopy (A and B) or flow cytometry (C and D) analysis of cholesterol uptake by Dil-OxLDL in WT and RBP4-deficient HEK293T cells or BMDMs. Scale bars, 100 μm. Statistics of mean fluorescence intensity was calculated by Image J software (A and B, right) or Flow Jo software (C and D, right). (E, F) Flow cytometry analysis of cholesterol uptake by Dil-OxLDL in WT, RBP4-deficient and CD36 overexpressing RBP4-deficient HEK293T cells (E) and BMDMs (F). Mean fluorescence intensities were quantified with Flow Jo software. (G, H) Flow cytometry analysis of SA expression in HEK293T cells (G, upper) transfected with hCD36 plasmid or in stable CD36-overexpressing iBMDMs (H, upper). Cells were left untreated or incubated with cholesterol for 1 hour at 37°C, followed by staining with SNA or MAL. Mean fluorescence intensities were quantified by Flow Jo software (lower panels). (I) Confocal microscopy analysis of SA expression and distribution in WT and CD36-overexpressing iBMDMs. Cells were left untreated or incubated with cholesterol for 1 hour at 37°C, followed by staining with SNA or MAL (green). Cell membranes were stained with Dil dye (red), and nuclei were counterstained with DAPI (blue). Data are representative (A-F, left, G, H, upper and I) or pooled from at least three independent experiments (A-F, right, G and H, lower, mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001 (Student’s t -test).

Techniques: Confocal Microscopy, Flow Cytometry, Fluorescence, Software, Expressing, Transfection, Plasmid Preparation, Incubation, Staining

(A, B) Flow cytometry analysis of α-2,3-linked SA or α-2,6-linked SA in WT, RBP4-deficient and CD36 overexpressing RBP4-deficient HEK293T cells, as wells as murine BMDMs transduced with CD36 retrovirus. Mean fluorescence intensities were quantified with FlowJo software. (C, D) qPCR analysis of vRNA levels of the NP gene or NP and M1 mRNA expression in HEK293T cells (C) or BMDMs (D) infected with IAV WSN strain (MOI = 5) during the viral attachment stage. (E) Flow cytometry analysis of α-2,3-linked SA or α-2,6-linked SA in WT and stable CD36-overexpressing iBMDMs cultured in serum-free medium. Cells were cultured with serum-free medium for 6 hours and subsequently stained with Lectins. Mean fluorescence intensities were quantified with FlowJo software. Data are pooled from three independent experiments (A-E, mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student’s t -test).

Journal: PLOS Pathogens

Article Title: Retinol binding protein 4 enhances cellular cholesterol uptake to facilitate influenza A virus infection

doi: 10.1371/journal.ppat.1013623

Figure Lengend Snippet: (A, B) Flow cytometry analysis of α-2,3-linked SA or α-2,6-linked SA in WT, RBP4-deficient and CD36 overexpressing RBP4-deficient HEK293T cells, as wells as murine BMDMs transduced with CD36 retrovirus. Mean fluorescence intensities were quantified with FlowJo software. (C, D) qPCR analysis of vRNA levels of the NP gene or NP and M1 mRNA expression in HEK293T cells (C) or BMDMs (D) infected with IAV WSN strain (MOI = 5) during the viral attachment stage. (E) Flow cytometry analysis of α-2,3-linked SA or α-2,6-linked SA in WT and stable CD36-overexpressing iBMDMs cultured in serum-free medium. Cells were cultured with serum-free medium for 6 hours and subsequently stained with Lectins. Mean fluorescence intensities were quantified with FlowJo software. Data are pooled from three independent experiments (A-E, mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student’s t -test).

Techniques: Flow Cytometry, Transduction, Fluorescence, Software, Expressing, Infection, Cell Culture, Staining

(A) Experimental scheme for lentiviral transduction and influenza virus infection in mice. WT and RBP4-deficient mice were intravenously injected with lentivirus (10 9 PFU in 200 μL per mouse) followed by infection with 10 4 PFU of IAV (WSN strain) 5 days later. Lungs were collected 3 days post-IAV infection. (B) qPCR analysis of CD36 mRNA levels in lung tissues from WT, RBP4-deficient, and CD36-overexpressing RBP4-deficient mice as treated in (A). (C) Body weight changes of indicated mouse genotypes at day 3 post-IAV infection. (D) Plaque assay analysis of virus titer in lung tissues from mice described in (A). (E, F) Immunofluorescence images (E, left) and quantitative analysis of NP protein intensity (E, right) or immunoblotting analysis of M1, NP and CD36 protein expression (F) in lung tissues from the mice described in (A). Mean fluorescence intensity was determined by Image J software (E, right). Scale bars, 100 μm. (G, H) Representative H&E-stained lung sections (G) and corresponding histopathological scores (H) from indicated groups. Each dot in (B-D, H) represents an individual mouse. (I) Proposed model of RBP4-mediated promotion of influenza virus infection. Created in BioRender. Huang, L. (2025) https://BioRender.com/rll2ll1 . Data are representative of two independent experiments (E-G). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student’s t -test).

Journal: PLOS Pathogens

Article Title: Retinol binding protein 4 enhances cellular cholesterol uptake to facilitate influenza A virus infection

doi: 10.1371/journal.ppat.1013623

Figure Lengend Snippet: (A) Experimental scheme for lentiviral transduction and influenza virus infection in mice. WT and RBP4-deficient mice were intravenously injected with lentivirus (10 9 PFU in 200 μL per mouse) followed by infection with 10 4 PFU of IAV (WSN strain) 5 days later. Lungs were collected 3 days post-IAV infection. (B) qPCR analysis of CD36 mRNA levels in lung tissues from WT, RBP4-deficient, and CD36-overexpressing RBP4-deficient mice as treated in (A). (C) Body weight changes of indicated mouse genotypes at day 3 post-IAV infection. (D) Plaque assay analysis of virus titer in lung tissues from mice described in (A). (E, F) Immunofluorescence images (E, left) and quantitative analysis of NP protein intensity (E, right) or immunoblotting analysis of M1, NP and CD36 protein expression (F) in lung tissues from the mice described in (A). Mean fluorescence intensity was determined by Image J software (E, right). Scale bars, 100 μm. (G, H) Representative H&E-stained lung sections (G) and corresponding histopathological scores (H) from indicated groups. Each dot in (B-D, H) represents an individual mouse. (I) Proposed model of RBP4-mediated promotion of influenza virus infection. Created in BioRender. Huang, L. (2025) https://BioRender.com/rll2ll1 . Data are representative of two independent experiments (E-G). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 (Student’s t -test).

Techniques: Transduction, Virus, Infection, Injection, Plaque Assay, Immunofluorescence, Western Blot, Expressing, Fluorescence, Software, Staining

Effects of mangiferin (MGF) and T0901317 (T0) on inhibition of AS progression. Apoe −/− mice fed with high fat diet (HFD) in four groups (n = 10/group) received the following treatment for 16 weeks. Ctrl: vehicle; T0: oral gavage of T0 (1 mg∙kg −1 bodyweight/day); MGF: oral gavage of MGF (200 mg kg −1 bodyweight/day); T0 + MGF: oral gavage of T0 and MGF. After treatment, aortas were collected for the following assays. A Lesions in en face aorta were determined by Oil Red O staining and lesion areas were expressed as % of total en face aorta areas. Scale bar, 5 mm. *** p < 0.001, ** p < 0.01, * p < 0.05, NS: not significant (n = 10). B Sinus lesions in aortic root were determined by Oil Red O staining and lesion areas were expressed as μm 2 /section. Scale bar, 400 μm. * p < 0.05 (n = 9). C Collagen content areas were determined by Masson staining of aortic root cross sections and quantified by a computer-assisted image analysis protocol (n = 3). Scale bar, 100 μm. D Expression of α-SMA (stained with red fluorescent color) was determined by immunofluorescent staining of aortic root cross sections and quantified by a computer-assisted image analysis protocol. Scale bar, 100 μm. *** p < 0.001, ** p < 0.01, * p < 0.05 (n = 3)

Journal: Chinese Medicine

Article Title: Combination of mangiferin and T0901317 targeting autophagy promotes cholesterol efflux from macrophage foam cell in atherosclerosis

doi: 10.1186/s13020-023-00876-9

Figure Lengend Snippet: Effects of mangiferin (MGF) and T0901317 (T0) on inhibition of AS progression. Apoe −/− mice fed with high fat diet (HFD) in four groups (n = 10/group) received the following treatment for 16 weeks. Ctrl: vehicle; T0: oral gavage of T0 (1 mg∙kg −1 bodyweight/day); MGF: oral gavage of MGF (200 mg kg −1 bodyweight/day); T0 + MGF: oral gavage of T0 and MGF. After treatment, aortas were collected for the following assays. A Lesions in en face aorta were determined by Oil Red O staining and lesion areas were expressed as % of total en face aorta areas. Scale bar, 5 mm. *** p < 0.001, ** p < 0.01, * p < 0.05, NS: not significant (n = 10). B Sinus lesions in aortic root were determined by Oil Red O staining and lesion areas were expressed as μm 2 /section. Scale bar, 400 μm. * p < 0.05 (n = 9). C Collagen content areas were determined by Masson staining of aortic root cross sections and quantified by a computer-assisted image analysis protocol (n = 3). Scale bar, 100 μm. D Expression of α-SMA (stained with red fluorescent color) was determined by immunofluorescent staining of aortic root cross sections and quantified by a computer-assisted image analysis protocol. Scale bar, 100 μm. *** p < 0.001, ** p < 0.01, * p < 0.05 (n = 3)

Article Snippet: Primary rabbit polyclonal antibodies against α-SMA (14395), CD36 (18836), Beclin1 (11306), ATG5 (10181), and ATG7 (10088) were purchased from Proteintech Group, Inc. (Rosemont, IL, USA).

Techniques: Inhibition, Staining, Expressing

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