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Proteintech antibodies hsp70

In vivo ALI therapy evaluation. A) Time schedule of in vivo animal experiment. B) Macroscopic observation in the lung tissue of treated rats. C) Wet/dry ratio in the lung tissue of treated rats. D) Inflammatory factors expression levels in the blood of treated rats. E) Inflammatory factors expression levels in the lung tissue of treated rats. F) ROS levels in the lung tissue of treated rats. (Scale bar = 50 μm) G) H&E staining images in the lung tissue of treated rats. (Scale bar = 100 μm) H) TNF-α expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (I). J) <t>HSP70</t> expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (K). L) CD31 expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (M). The corresponding groups were: rats without treatments (sham group), and rats pretreated with LPS followed by IT administration of PBS (ALI group), CPs (CPs), CPs@SS31 (CPs@SS31) and CPs@SS31 combining with NIR irradiation (CPs@SS31+NIR). (”∗” symbol compared with sham group, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 and ∗∗∗∗p < 0.0001).

Antibodies Hsp70, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 450 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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antibodies hsp70 - by Bioz Stars, 2026-06

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1) Product Images from "Near infrared enhanced palladium loaded siraitia grosvenorii carbon dots amplify mitophagy for acute lung injury immunotherapy"

Article Title: Near infrared enhanced palladium loaded siraitia grosvenorii carbon dots amplify mitophagy for acute lung injury immunotherapy

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.040

Figure Legend Snippet: In vivo ALI therapy evaluation. A) Time schedule of in vivo animal experiment. B) Macroscopic observation in the lung tissue of treated rats. C) Wet/dry ratio in the lung tissue of treated rats. D) Inflammatory factors expression levels in the blood of treated rats. E) Inflammatory factors expression levels in the lung tissue of treated rats. F) ROS levels in the lung tissue of treated rats. (Scale bar = 50 μm) G) H&E staining images in the lung tissue of treated rats. (Scale bar = 100 μm) H) TNF-α expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (I). J) HSP70 expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (K). L) CD31 expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (M). The corresponding groups were: rats without treatments (sham group), and rats pretreated with LPS followed by IT administration of PBS (ALI group), CPs (CPs), CPs@SS31 (CPs@SS31) and CPs@SS31 combining with NIR irradiation (CPs@SS31+NIR). (”∗” symbol compared with sham group, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 and ∗∗∗∗p < 0.0001).

Techniques Used: In Vivo, Expressing, Staining, Irradiation

Image Search Results

Journal: Bioactive Materials

Article Title: Near infrared enhanced palladium loaded siraitia grosvenorii carbon dots amplify mitophagy for acute lung injury immunotherapy

doi: 10.1016/j.bioactmat.2026.02.040

Figure Lengend Snippet: In vivo ALI therapy evaluation. A) Time schedule of in vivo animal experiment. B) Macroscopic observation in the lung tissue of treated rats. C) Wet/dry ratio in the lung tissue of treated rats. D) Inflammatory factors expression levels in the blood of treated rats. E) Inflammatory factors expression levels in the lung tissue of treated rats. F) ROS levels in the lung tissue of treated rats. (Scale bar = 50 μm) G) H&E staining images in the lung tissue of treated rats. (Scale bar = 100 μm) H) TNF-α expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (I). J) HSP70 expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (K). L) CD31 expression levels in the lung tissue of treated rats, (Scale bar = 100 μm) and the corresponding quantified results (M). The corresponding groups were: rats without treatments (sham group), and rats pretreated with LPS followed by IT administration of PBS (ALI group), CPs (CPs), CPs@SS31 (CPs@SS31) and CPs@SS31 combining with NIR irradiation (CPs@SS31+NIR). (”∗” symbol compared with sham group, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 and ∗∗∗∗p < 0.0001).

Article Snippet: And then, the cells were incubated with primary antibodies (anti-IL-6, TNF-α, CD206, CD86, CD31, HSP70 and PINK1, 1 : 200, Proteintech, USA) overnight.

Techniques: In Vivo, Expressing, Staining, Irradiation

PVPAC/AF co-culture model confirms that PVPAC-derived exosomes mediated intercellular communication. (A) Schematic diagram of primary PVPAC/AF cells culture with subsequent exosome isolation. (B) PVPAC/AF cells co-culture model. (B1) Schematic of the transwell-based co-culture setup. (B2) Representative TEM micrograph showing exosome morphology, scale bar = 100 nm. (B3) NTA-derived size distribution and concentration profiles of isolated exosomes. (B4) Crystal violet assay assessing cell proliferation under different glucose conditions, scale bar = 200 μm. (B5 and B6) Quantitative histograms corresponding to (B3) and (B4), respectively. Data are compared across mono-vs. co-culture systems under normal (NG) or high glucose (HG). vs NG + AF group, ∗P < 0.05, ∗∗P < 0.01. (C) Confocal microscopy tracking exosome uptake. Scale bar = 50 μm. (C1) PKH67-labeled PVPAC-derived exosomes (green) enriched in PVPAC cytoplasm. (C2) PKH67-labeled AF-derived exosomes abundant within AF cytoplasm. (C3) Time-course imaging displayed PVPAC-Exo accumulation in AFs, peaking at 4 h. (D) Quantification of migration and proliferation capacities in AFs after 24-h treatment with PVPAC-Exo (1 × 10 6 particles/mL), using PBS as a vehicle control, scale bar = 200 μm. (E) Impact of NG, HG, and GW4869 on exosome biology, scale bar = 100 nm. (E1) Morphology assessed by TEM. (E2) Proliferation measured via crystal violet. (E3) Western blot quantification of vimentin and exosomal markers (CD63, TSG101) in AFs. (F) RT-PCR analysis of circEif3c and miR-96–5p in AFs and PVPACs after 24 h NG vs. HG. HG induced highest circEif3c and lowest miR-96–5p expression in PVPACs. (G–K) Systematic comparison of exosomal protein signatures across culture modalities. (G1)Single-cell culture. (G2)Dual-cell co-culture. (G3) Co-culture pre-loaded with 1 × 10 6 /mL PVPAC-Exo. (H–K) Bar graphs present mean ± SD. n (the number of experiments) = 3; one-way ANOVA with Dunnett's post-test. ∗vs. respective NG group: ∗P < 0.05, ∗∗P < 0.01; vs. respective HG group: #P < 0.05, ##P < 0.01.

Journal: Non-coding RNA Research

Article Title: CircEif3c/miR-96–5p/PHF20L1/MEOX2 axis in perivascular preadipocyte exosomes mediates fibroblast dysfunction and vascular remodeling

doi: 10.1016/j.ncrna.2026.01.006

Figure Lengend Snippet: PVPAC/AF co-culture model confirms that PVPAC-derived exosomes mediated intercellular communication. (A) Schematic diagram of primary PVPAC/AF cells culture with subsequent exosome isolation. (B) PVPAC/AF cells co-culture model. (B1) Schematic of the transwell-based co-culture setup. (B2) Representative TEM micrograph showing exosome morphology, scale bar = 100 nm. (B3) NTA-derived size distribution and concentration profiles of isolated exosomes. (B4) Crystal violet assay assessing cell proliferation under different glucose conditions, scale bar = 200 μm. (B5 and B6) Quantitative histograms corresponding to (B3) and (B4), respectively. Data are compared across mono-vs. co-culture systems under normal (NG) or high glucose (HG). vs NG + AF group, ∗P < 0.05, ∗∗P < 0.01. (C) Confocal microscopy tracking exosome uptake. Scale bar = 50 μm. (C1) PKH67-labeled PVPAC-derived exosomes (green) enriched in PVPAC cytoplasm. (C2) PKH67-labeled AF-derived exosomes abundant within AF cytoplasm. (C3) Time-course imaging displayed PVPAC-Exo accumulation in AFs, peaking at 4 h. (D) Quantification of migration and proliferation capacities in AFs after 24-h treatment with PVPAC-Exo (1 × 10 6 particles/mL), using PBS as a vehicle control, scale bar = 200 μm. (E) Impact of NG, HG, and GW4869 on exosome biology, scale bar = 100 nm. (E1) Morphology assessed by TEM. (E2) Proliferation measured via crystal violet. (E3) Western blot quantification of vimentin and exosomal markers (CD63, TSG101) in AFs. (F) RT-PCR analysis of circEif3c and miR-96–5p in AFs and PVPACs after 24 h NG vs. HG. HG induced highest circEif3c and lowest miR-96–5p expression in PVPACs. (G–K) Systematic comparison of exosomal protein signatures across culture modalities. (G1)Single-cell culture. (G2)Dual-cell co-culture. (G3) Co-culture pre-loaded with 1 × 10 6 /mL PVPAC-Exo. (H–K) Bar graphs present mean ± SD. n (the number of experiments) = 3; one-way ANOVA with Dunnett's post-test. ∗vs. respective NG group: ∗P < 0.05, ∗∗P < 0.01; vs. respective HG group: #P < 0.05, ##P < 0.01.

Article Snippet: Antibodies against MEOX2 (1:1500, #ab262916, Abcam, UK), PHF20L1 (1:1500, #ab118190, Abcam, UK), β-actin (#AC004, 1:5000, ABclone, Wuhan), Bcl-2 (1:2000, #ab182858, Abcam, UK), N-cadherin (1:1500, Abcam, UK), vimentin (1:2000, #ab92547, Abcam, UK), Anti-CD63 (1:1000, #ab315108, Abcam, UK), and TSG101 (1:2000, #28283-1-AP, Proteintech, USA) were purchased.

Techniques: Co-Culture Assay, Derivative Assay, Isolation, Concentration Assay, Crystal Violet Assay, Confocal Microscopy, Labeling, Imaging, Migration, Control, Western Blot, Reverse Transcription Polymerase Chain Reaction, Expressing, Comparison, Single Cell

In vitro evaluation of foam cell lipid accumulation and lipophagy activation following OPN-HMCN@MLT treatment. ( A - C ) ORO and BODIPY staining images and corresponding quantification of ORO and BODIPY positive areas of RAW264.7 cells under different stimulations (n = 5, scale bar for ORO: 100 μm, scale bar for BODIPY: 20 μm). ( D ) Bio-TEM images of RAW264.7 cells post various treatments (n = 5, scale bars 1.0 μm). Green arrows indicate nanoparticles. ( E , F ) Morphometric analysis determined the mean number and area (μm 2 ) of LDs per cell section. ( G ) Confocal images depicting lipophagy flux in foam cells following different treatments (n = 5 biological replicates, scale bars: 10 μm). ( H - J ) The quantities of acidified autophagosomes (GFP-RFP+), neutral autophagosomes (GFP + RFP+), and LDs labeled with BODIPY were measured per cell for each condition. (K to N) Representative Western blot images and quantitative analysis of LC3, LAMP1, and P62 expression in foam cells. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

Journal: Bioactive Materials

Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

doi: 10.1016/j.bioactmat.2026.02.041

Figure Lengend Snippet: In vitro evaluation of foam cell lipid accumulation and lipophagy activation following OPN-HMCN@MLT treatment. ( A - C ) ORO and BODIPY staining images and corresponding quantification of ORO and BODIPY positive areas of RAW264.7 cells under different stimulations (n = 5, scale bar for ORO: 100 μm, scale bar for BODIPY: 20 μm). ( D ) Bio-TEM images of RAW264.7 cells post various treatments (n = 5, scale bars 1.0 μm). Green arrows indicate nanoparticles. ( E , F ) Morphometric analysis determined the mean number and area (μm 2 ) of LDs per cell section. ( G ) Confocal images depicting lipophagy flux in foam cells following different treatments (n = 5 biological replicates, scale bars: 10 μm). ( H - J ) The quantities of acidified autophagosomes (GFP-RFP+), neutral autophagosomes (GFP + RFP+), and LDs labeled with BODIPY were measured per cell for each condition. (K to N) Representative Western blot images and quantitative analysis of LC3, LAMP1, and P62 expression in foam cells. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

Article Snippet: To block nonspecific binding, membranes were incubated with 5% skim milk for 1 h. Thereafter, membranes were incubated overnight at 4 °C with primary antibodies against ABCA1, ABCG1, ACOX1, CPT1A, LC3 (ab192890, 1:2000, abcam), LAMP1 (84658-5-RR, 1:8000, Proteintech), PPARα (66826-1-Ig, 1:3000, Proteintech), PPARγ (66936-1-Ig, 1:10000, Proteintech), P62 (18420-1-AP, 1:10000, Proteintech), MCAD (55210-1-AP, 1:3000, Proteintech), LCAD (17526-1-AP, 1:10000, Proteintech), tubulin (80762-1-RR, 1:10000, Proteintech), GAPDH (60004-1-Ig, 1:50000, Proteintech), and β-actin (66009-1-Ig, 1:20000, Proteintech).

Techniques: In Vitro, Activation Assay, Staining, Labeling, Western Blot, Expressing

Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

Journal: Bioactive Materials

Article Title: A foam cell-targeted lipophagy restoration strategy stabilizes vulnerable atherosclerotic plaques

doi: 10.1016/j.bioactmat.2026.02.041

Figure Lengend Snippet: Schematic of the anti-atherosclerotic mechanism of OPN-HMCN@MLT. ( A ) The study commenced with the synthesis of mesoporous carbon nanospheres (MCN) functionalized with an OPN-binding peptide and hyaluronic acid to construct the OPN-HMCN nanoplatform. The OPN-binding peptide was designed to recognize OPN enriched in the extracellular matrix and on the surface of foam cells, thereby enabling selective accumulation in OPN-rich pathological regions. Following OPN recognition, OPN-HMCN@MLT undergoes CD44-dependent endocytosis. Melatonin (MLT), a lipid autophagy–promoting agent, was subsequently encapsulated within the nanocarrier to form OPN-HMCN@MLT. Firstly, the released MLT can bind to and upregulate the expression of PPARα and PPARγ, which then promote the expression of downstream genes (ABCA1, ABCG1, ACOX-1, and CTP1A) and trigger the lipophagy. ( B ) Subsequently, its lipophagy-enhancing effects, including ABCA1/G1-mediated cholesterol efflux and CTP1A/ACOX-1-mediated mitochondrial fatty acid oxidation, were studied to confirm the reversal of foam cell formation. ( C ) These effects eventually promote foam cells to reverse into macrophages. Abbreviations: MCN, mesoporous carbon nanoparticle; OPN, osteopontin; MLT, melatonin; LDL, low-density lipoprotein; ox-LDL, oxidized low-density lipoprotein; PA, Photoacoustic.

Techniques: Binding Assay, Construct, Expressing

Senescent Microenvironment-Educated Mesenchymal Stem Cells Release High-Affinity Senescent NPC Domesticated Extracellular Vesicles. (A) Schematic diagram of the experimental setup for educating MSCs with SASP-CM to generate D-EVs versus N-EVs. (B) Confocal microscopy images showing different EVs internalization by senescent NPCs after 12 h in vitro. (C) Flow cytometry and quantification analysis of different EVs uptake by senescent NPCs. (D) In vivo validation of the senescent niche. Representative fluorescence images following injection of senescence-tracer (Red). (E) In vivo PKH26-labeled D-EVs tracking. (F) Representative SA-β-Gal images and quantification of MSCs treated with SASP-CM or not. (G) Gene Ontology (GO) analysis confirming enrichment of external encapsulating structure organization and cytokine production in Biological Process (BP) categories. (H) Heatmap indicating gene expression associated with EVs biogenesis within D-MSCs and N-MSCs. (I) Heatmap indicating gene expression associated with cytokine production within D-MSCs and N-MSCs. (J and L) Gene Ontology (GO) analysis confirming enrichment of terms related to vesicle organization and transport in the Cellular Component (CC) categories. (K) Western blot analysis confirmed core senescence markers p16 and p21 and DNA damage marker γ-H2AX in N-MSC and D-MSC. (M) Western blot analysis confirmed the expression of CD9, CD63, TSG101, Calnexin, and GM130 in MSC-EVs, N-EVs, or D-EVs. (N) TEM images showing the morphology and size of MSC-derived EVs, N-EVs, and D-EVs. (O) NTA shows size distribution in MSC-EVs, N-EVs, or D-EVs. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

Article Title: Microenvironment-educated MSC-EVs loaded injectable smart hydrogel for targeting senescent nucleus pulposus cells and inhibiting ferroptosis against intervertebral disc degeneration

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: Senescent Microenvironment-Educated Mesenchymal Stem Cells Release High-Affinity Senescent NPC Domesticated Extracellular Vesicles. (A) Schematic diagram of the experimental setup for educating MSCs with SASP-CM to generate D-EVs versus N-EVs. (B) Confocal microscopy images showing different EVs internalization by senescent NPCs after 12 h in vitro. (C) Flow cytometry and quantification analysis of different EVs uptake by senescent NPCs. (D) In vivo validation of the senescent niche. Representative fluorescence images following injection of senescence-tracer (Red). (E) In vivo PKH26-labeled D-EVs tracking. (F) Representative SA-β-Gal images and quantification of MSCs treated with SASP-CM or not. (G) Gene Ontology (GO) analysis confirming enrichment of external encapsulating structure organization and cytokine production in Biological Process (BP) categories. (H) Heatmap indicating gene expression associated with EVs biogenesis within D-MSCs and N-MSCs. (I) Heatmap indicating gene expression associated with cytokine production within D-MSCs and N-MSCs. (J and L) Gene Ontology (GO) analysis confirming enrichment of terms related to vesicle organization and transport in the Cellular Component (CC) categories. (K) Western blot analysis confirmed core senescence markers p16 and p21 and DNA damage marker γ-H2AX in N-MSC and D-MSC. (M) Western blot analysis confirmed the expression of CD9, CD63, TSG101, Calnexin, and GM130 in MSC-EVs, N-EVs, or D-EVs. (N) TEM images showing the morphology and size of MSC-derived EVs, N-EVs, and D-EVs. (O) NTA shows size distribution in MSC-EVs, N-EVs, or D-EVs. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: After blocked with 5% non-fat milk for 2 h at room temperature, the membranes were incubated with primary antibodies against GAPDH (1:5000, 104941-AP, Proteintech), TSG101 (1:1000, DF8427, Affinity), CD9 (1:1000, AF5139, Affinity), CD63 (1:2000, 25682-1-AP, Proteintech), Calnexin (1:5000, 10427-2-AP, Proteintech), GM130 (1:20000, 11308-1-AP, Proteintech), CXCR3 (1:5000, 26756-1-AP, Proteintech), CXCL10 (1:2000, 10937-1-AP, Proteintech), MMP3 (1:2000, 17873-1-AP, Proteintech), ADAMTS5 (DF13268, Affinity), P16 (AF5484, Affinity), P21 (10355-1-AP, Proteintech), GPX4 (1:1000, 381958, Zen-bio), SLC7A11 (1:1000, 26864-1-AP, Proteintech), ACSL4 (1:5000, 22401-1-AP, Proteintech) and Tubulin (1:10000, T40103 , Abmart) overnight at 4 °C.

Techniques: Confocal Microscopy, In Vitro, Flow Cytometry, In Vivo, Biomarker Discovery, Fluorescence, Injection, Labeling, Gene Expression, Western Blot, Marker, Expressing, Derivative Assay

D-EVs Alleviate Cellular Senescence and Restore ECM anabolic/catabolic metabolism in Senescent NPCs. (A) The CCK8 assay was used to determine D-EVs concentrations on cell viability. (B) Flow cytometry analysis of proliferative capacity in the above group, and (C) quantitative analysis. (D) Representative ROS images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869. (E) Representative SA-β-Gal images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869, and (F) quantitative analysis. (G) Confocal analysis of γ-H2A with IF staining depicting DNA damage in the control, TBHP, N-Evs, or D-EVs group. (H) WB analysis of ECM metabolism–related and aging-related proteins in NPCs following treatment with Control, TBHP, N-Evs, or D-EVs. (I) Western blot analysis of p53, p21, and p16 in senescent NPCs treated with D-EVs, D-CM, or D-CM EV-dep . (J) Confocal analysis of COL2 with IF staining in the control, TBHP, N-EVs, or D-EVs group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: D-EVs Alleviate Cellular Senescence and Restore ECM anabolic/catabolic metabolism in Senescent NPCs. (A) The CCK8 assay was used to determine D-EVs concentrations on cell viability. (B) Flow cytometry analysis of proliferative capacity in the above group, and (C) quantitative analysis. (D) Representative ROS images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869. (E) Representative SA-β-Gal images of senescent NPCs treated with N-EVs, D-EVs, or D-EVs + GW4869, and (F) quantitative analysis. (G) Confocal analysis of γ-H2A with IF staining depicting DNA damage in the control, TBHP, N-Evs, or D-EVs group. (H) WB analysis of ECM metabolism–related and aging-related proteins in NPCs following treatment with Control, TBHP, N-Evs, or D-EVs. (I) Western blot analysis of p53, p21, and p16 in senescent NPCs treated with D-EVs, D-CM, or D-CM EV-dep . (J) Confocal analysis of COL2 with IF staining in the control, TBHP, N-EVs, or D-EVs group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Techniques: CCK-8 Assay, Flow Cytometry, Staining, Control, Western Blot

D-EVs Counteract NPC Senescence by Suppressing Ferroptosis. (A) KEGG pathway analysis of DEGs in senescent NPCs following treatment with D-EVs or not. (B-C) GSEA plots showing significant enrichment of ferroptosis and cell cycle in senescent NPCs. (D-E) Heatmap quantification of key genes involved in ferroptosis and cell cycle. (F) Western blot analysis of key ferroptosis (GPX4, SLC7A11, ACSL4) and senescence (p21, P16) markers in NPCs following treatment with different experimental conditions. (G) Representative images of C11-BODIPY 581/591 staining to detect lipid peroxidation (green) in the control, TBHP, Era, Era + Fer-1, or TBHP + Fer-1 groups. (H-I) Quantitative assessment of malondialdehyde (MDA) levels (H) and glutathione (GSH) levels (I) in the control, TBHP, N-EVs, D-EVs, or D-EVs + Era groups. (J) Western blot analysis of key ferroptosis (GPX4, SLC7A11, ACSL4) and senescence (p21, P16) markers in NPCs following treatment with PBS, N-EVs, D-EVs, or D-EVs + Era. (K) Confocal analysis of GPX4 with IF staining in the control, TBHP, N-Evs, D-EVs, and D-EVs + Era group. (L) Flow cytometry analysis of cell cycle distribution in the above experimental conditions. Statistical comparisons were performed between the experimental group and the TBHP-induced group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: D-EVs Counteract NPC Senescence by Suppressing Ferroptosis. (A) KEGG pathway analysis of DEGs in senescent NPCs following treatment with D-EVs or not. (B-C) GSEA plots showing significant enrichment of ferroptosis and cell cycle in senescent NPCs. (D-E) Heatmap quantification of key genes involved in ferroptosis and cell cycle. (F) Western blot analysis of key ferroptosis (GPX4, SLC7A11, ACSL4) and senescence (p21, P16) markers in NPCs following treatment with different experimental conditions. (G) Representative images of C11-BODIPY 581/591 staining to detect lipid peroxidation (green) in the control, TBHP, Era, Era + Fer-1, or TBHP + Fer-1 groups. (H-I) Quantitative assessment of malondialdehyde (MDA) levels (H) and glutathione (GSH) levels (I) in the control, TBHP, N-EVs, D-EVs, or D-EVs + Era groups. (J) Western blot analysis of key ferroptosis (GPX4, SLC7A11, ACSL4) and senescence (p21, P16) markers in NPCs following treatment with PBS, N-EVs, D-EVs, or D-EVs + Era. (K) Confocal analysis of GPX4 with IF staining in the control, TBHP, N-Evs, D-EVs, and D-EVs + Era group. (L) Flow cytometry analysis of cell cycle distribution in the above experimental conditions. Statistical comparisons were performed between the experimental group and the TBHP-induced group. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Techniques: Western Blot, Staining, Control, Flow Cytometry

D-EVs Deliver GPX4 to Inhibit Ferroptosis in Senescent NPCs. (A) Representative Senescent-Tracker images of NPCs treated with N-EVs, D-EVs, Era, and D-Evs sh-CXCL10 . (B) Volcano plot of transcriptomic data comparing D-MSC and N-MSC. (C) KEGG pathway analysis of DEGs in D-MSCs versus N-MSCs. (D) Volcano plot of proteomic data comparing D-EVs and N-EVs. (E) KEGG pathway analysis of transcriptomic and proteomic data integration. (F) A Venn diagram illustrating the intersection of genes from the D-MSC transcriptome, the D-EVs proteome, and the ferroptosis-related gene set. (G) Bar graph showing the relative expression levels of core overlapping genes identified in (F). (H) MS analysis revealed that GPX4 is enriched in the D-EVs proteome. (I) Western blot analysis confirming GPX4 protein in D-EVs and N-EVs. (J) Western blot analysis of key senescence (p21, P16) markers in NPCs following treatment with PBS or N-EVs with CXCL10 or GPX4 knockout. (K) Representative images of EdU depicting cell proliferation ability in the control, TBHP, D-EVs, D-EVs sh-CXCL10 , D-EVs sh-GPX4 , and D-EVs sh-CXCL10+GPX4 groups. (L-M) Confocal images showing GPX4 delivery from different EVs to senescent NPCs at 12h and 24h co-culture, and (N) colocalization analysis. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Journal: Bioactive Materials

doi: 10.1016/j.bioactmat.2026.02.030

Figure Lengend Snippet: D-EVs Deliver GPX4 to Inhibit Ferroptosis in Senescent NPCs. (A) Representative Senescent-Tracker images of NPCs treated with N-EVs, D-EVs, Era, and D-Evs sh-CXCL10 . (B) Volcano plot of transcriptomic data comparing D-MSC and N-MSC. (C) KEGG pathway analysis of DEGs in D-MSCs versus N-MSCs. (D) Volcano plot of proteomic data comparing D-EVs and N-EVs. (E) KEGG pathway analysis of transcriptomic and proteomic data integration. (F) A Venn diagram illustrating the intersection of genes from the D-MSC transcriptome, the D-EVs proteome, and the ferroptosis-related gene set. (G) Bar graph showing the relative expression levels of core overlapping genes identified in (F). (H) MS analysis revealed that GPX4 is enriched in the D-EVs proteome. (I) Western blot analysis confirming GPX4 protein in D-EVs and N-EVs. (J) Western blot analysis of key senescence (p21, P16) markers in NPCs following treatment with PBS or N-EVs with CXCL10 or GPX4 knockout. (K) Representative images of EdU depicting cell proliferation ability in the control, TBHP, D-EVs, D-EVs sh-CXCL10 , D-EVs sh-GPX4 , and D-EVs sh-CXCL10+GPX4 groups. (L-M) Confocal images showing GPX4 delivery from different EVs to senescent NPCs at 12h and 24h co-culture, and (N) colocalization analysis. The data were presented as mean ± SD. n = 3, ns, not significant; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Techniques: Expressing, Western Blot, Knock-Out, Control, Co-Culture Assay

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