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Thermo Fisher serum free dmem
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MedChemExpress fluorescein phalloidin
Good biocompatibility of GRb1@LEVs-cRGD in vitro and in vivo . (a-c) CCK-8 assays in RAW264.7, MLE-12 and HUVEC cells, respectively (n = 3). (d) Live/dead cell staining in RAW264.7, MLE-12 and HUVEC cells. Green, Calcein AM staining for live cells. Red, propidium iodide staining for dead cells (n = 3). (e) Cell skeleton staining in HUVECs. Green, FITC <t>phalloidine.</t> Blue, DAPI. (f) Blood routine and biochemical indexes ( n = 3). (g) Representative TUNEL staining of lung tissues from GRb1@LEVs-cRGD and control groups (n = 3). (h) Histopathological examination by H&E staining of major organs (n = 3).
Fluorescein Phalloidin, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Antibodies Inc fluoresceinated goat anti-chicken igy secondary antibody
Good biocompatibility of GRb1@LEVs-cRGD in vitro and in vivo . (a-c) CCK-8 assays in RAW264.7, MLE-12 and HUVEC cells, respectively (n = 3). (d) Live/dead cell staining in RAW264.7, MLE-12 and HUVEC cells. Green, Calcein AM staining for live cells. Red, propidium iodide staining for dead cells (n = 3). (e) Cell skeleton staining in HUVECs. Green, FITC <t>phalloidine.</t> Blue, DAPI. (f) Blood routine and biochemical indexes ( n = 3). (g) Representative TUNEL staining of lung tissues from GRb1@LEVs-cRGD and control groups (n = 3). (h) Histopathological examination by H&E staining of major organs (n = 3).
Fluoresceinated Goat Anti Chicken Igy Secondary Antibody, supplied by Antibodies Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Thermo Fisher fluorescein conjugated wheat germ agglutinin wga stain
Good biocompatibility of GRb1@LEVs-cRGD in vitro and in vivo . (a-c) CCK-8 assays in RAW264.7, MLE-12 and HUVEC cells, respectively (n = 3). (d) Live/dead cell staining in RAW264.7, MLE-12 and HUVEC cells. Green, Calcein AM staining for live cells. Red, propidium iodide staining for dead cells (n = 3). (e) Cell skeleton staining in HUVECs. Green, FITC <t>phalloidine.</t> Blue, DAPI. (f) Blood routine and biochemical indexes ( n = 3). (g) Representative TUNEL staining of lung tissues from GRb1@LEVs-cRGD and control groups (n = 3). (h) Histopathological examination by H&E staining of major organs (n = 3).
Fluorescein Conjugated Wheat Germ Agglutinin Wga Stain, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Valiant Co Ltd anti-human complement c3 goat igg fraction, fluorescein-conjugated
Good biocompatibility of GRb1@LEVs-cRGD in vitro and in vivo . (a-c) CCK-8 assays in RAW264.7, MLE-12 and HUVEC cells, respectively (n = 3). (d) Live/dead cell staining in RAW264.7, MLE-12 and HUVEC cells. Green, Calcein AM staining for live cells. Red, propidium iodide staining for dead cells (n = 3). (e) Cell skeleton staining in HUVECs. Green, FITC <t>phalloidine.</t> Blue, DAPI. (f) Blood routine and biochemical indexes ( n = 3). (g) Representative TUNEL staining of lung tissues from GRb1@LEVs-cRGD and control groups (n = 3). (h) Histopathological examination by H&E staining of major organs (n = 3).
Anti Human Complement C3 Goat Igg Fraction, Fluorescein Conjugated, supplied by Valiant Co Ltd, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Thermo Fisher fluorescein isothiocyanate fitc
Good biocompatibility of GRb1@LEVs-cRGD in vitro and in vivo . (a-c) CCK-8 assays in RAW264.7, MLE-12 and HUVEC cells, respectively (n = 3). (d) Live/dead cell staining in RAW264.7, MLE-12 and HUVEC cells. Green, Calcein AM staining for live cells. Red, propidium iodide staining for dead cells (n = 3). (e) Cell skeleton staining in HUVECs. Green, FITC <t>phalloidine.</t> Blue, DAPI. (f) Blood routine and biochemical indexes ( n = 3). (g) Representative TUNEL staining of lung tissues from GRb1@LEVs-cRGD and control groups (n = 3). (h) Histopathological examination by H&E staining of major organs (n = 3).
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MedChemExpress fluorescein isothiocyanate fitc dextran
Clinoptilolite zeolite reduces LPS-induced epithelial permeability in Caco-2 monolayers. Caco-2 cells were cultured on 0.4-µm Transwell inserts for 7 days to allow epithelial monolayer formation prior to treatment with lipopolysaccharide (LPS), clinoptilolite zeolite (ZEO), or combined LPS + ZEO conditions for 24 h. Epithelial permeability was subsequently evaluated using <t>FITC-dextran</t> (70 kDa) translocation across the epithelial barrier. Data are presented as relative fluorescence units (RFU) ± SD. Statistical significance was determined using an unpaired Student’s t-test.
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Thermo Fisher nhs fluorescein
SOS1 inhibition attenuates extracellular matrix deposition, stellate cell activation, and downstream signaling in LX2 hepatic stellate cells (A–D) Decellularized extracellular matrix (ECM) derived from activated LX2 cells treated with increasing concentrations of SOS1 inhibitor (SOS-I) and stained with <t>NHS-Fluorescein,</t> showing a progressive reduction in ECM deposition with SOS1 inhibition. (E) Representative immunoblot of fibrogenic markers (COL1A1, FN1, α-SMA, PDGFRB) with calnexin as loading control, demonstrating reduced protein expression following SOS-I treatment. (F–I) Quantitative analyses of fibrogenic and inflammatory readouts showing modulation of ECM-associated and signaling markers following SOS1 inhibition. (J–M) Immunofluorescence staining of extracellular matrix components, including collagen (green, J and K) and fibronectin (red, L and M), demonstrating reduced matrix deposition in SOS-I-treated cells. Nuclei are counterstained with DAPI (blue). (N and O) BODIPY staining of LX2 cells showing increased lipid droplet accumulation following SOS1 inhibition, consistent with partial reversion of stellate cell activation. (P and Q) Transwell migration assays demonstrating reduced migratory capacity of activated LX2 cells following SOS-I treatment. (R) Immunoblot analysis of pERK and total ERK in LX2 cells stimulated with PDGFB in the presence or absence of SOS-I, with calnexin as loading control, showing attenuation of PDGFB-induced ERK phosphorylation. (S) Immunoblot analysis of pERK and total ERK in LX2 cells treated with increasing concentrations of SOS-I, demonstrating dose-dependent reduction in ERK phosphorylation. (T) qRT-PCR confirmation of siRNA-mediated SOS1 knockdown using two independent siRNAs (13.1 and 13.2), with expression normalized to GAPDH. (U) Immunoblot analysis showing the effect of SOS1 knockdown on COL1A1 and IL-1β protein expression, with calnexin as loading control. Data are presented as mean ± SEM with individual data points shown. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01. Statistical analyses were performed using one-way ANOVA with Tukey’s post hoc test or two-tailed unpaired Student’s t test where appropriate. Data represent mean ± SEM from n = 3 independent experiments (LX-2 studies). Exact p values are shown in the graphs. Scale bars, 400 μm for ECM imaging in (A–D); 200 μm for extracellular collagen and fibronectin immunofluorescence images (J–M) and BODIPY staining (N and O); and 100 μm for transwell migration assay images (P and Q).
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MedChemExpress fluorescein tyramide
SOS1 inhibition attenuates extracellular matrix deposition, stellate cell activation, and downstream signaling in LX2 hepatic stellate cells (A–D) Decellularized extracellular matrix (ECM) derived from activated LX2 cells treated with increasing concentrations of SOS1 inhibitor (SOS-I) and stained with <t>NHS-Fluorescein,</t> showing a progressive reduction in ECM deposition with SOS1 inhibition. (E) Representative immunoblot of fibrogenic markers (COL1A1, FN1, α-SMA, PDGFRB) with calnexin as loading control, demonstrating reduced protein expression following SOS-I treatment. (F–I) Quantitative analyses of fibrogenic and inflammatory readouts showing modulation of ECM-associated and signaling markers following SOS1 inhibition. (J–M) Immunofluorescence staining of extracellular matrix components, including collagen (green, J and K) and fibronectin (red, L and M), demonstrating reduced matrix deposition in SOS-I-treated cells. Nuclei are counterstained with DAPI (blue). (N and O) BODIPY staining of LX2 cells showing increased lipid droplet accumulation following SOS1 inhibition, consistent with partial reversion of stellate cell activation. (P and Q) Transwell migration assays demonstrating reduced migratory capacity of activated LX2 cells following SOS-I treatment. (R) Immunoblot analysis of pERK and total ERK in LX2 cells stimulated with PDGFB in the presence or absence of SOS-I, with calnexin as loading control, showing attenuation of PDGFB-induced ERK phosphorylation. (S) Immunoblot analysis of pERK and total ERK in LX2 cells treated with increasing concentrations of SOS-I, demonstrating dose-dependent reduction in ERK phosphorylation. (T) qRT-PCR confirmation of siRNA-mediated SOS1 knockdown using two independent siRNAs (13.1 and 13.2), with expression normalized to GAPDH. (U) Immunoblot analysis showing the effect of SOS1 knockdown on COL1A1 and IL-1β protein expression, with calnexin as loading control. Data are presented as mean ± SEM with individual data points shown. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01. Statistical analyses were performed using one-way ANOVA with Tukey’s post hoc test or two-tailed unpaired Student’s t test where appropriate. Data represent mean ± SEM from n = 3 independent experiments (LX-2 studies). Exact p values are shown in the graphs. Scale bars, 400 μm for ECM imaging in (A–D); 200 μm for extracellular collagen and fibronectin immunofluorescence images (J–M) and BODIPY staining (N and O); and 100 μm for transwell migration assay images (P and Q).
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Image Search Results


Good biocompatibility of GRb1@LEVs-cRGD in vitro and in vivo . (a-c) CCK-8 assays in RAW264.7, MLE-12 and HUVEC cells, respectively (n = 3). (d) Live/dead cell staining in RAW264.7, MLE-12 and HUVEC cells. Green, Calcein AM staining for live cells. Red, propidium iodide staining for dead cells (n = 3). (e) Cell skeleton staining in HUVECs. Green, FITC phalloidine. Blue, DAPI. (f) Blood routine and biochemical indexes ( n = 3). (g) Representative TUNEL staining of lung tissues from GRb1@LEVs-cRGD and control groups (n = 3). (h) Histopathological examination by H&E staining of major organs (n = 3).

Journal: Bioactive Materials

Article Title: A safe and anti-inflammatory plant-derived nanovesicle platform for targeted delivery in acute lung injury

doi: 10.1016/j.bioactmat.2026.03.033

Figure Lengend Snippet: Good biocompatibility of GRb1@LEVs-cRGD in vitro and in vivo . (a-c) CCK-8 assays in RAW264.7, MLE-12 and HUVEC cells, respectively (n = 3). (d) Live/dead cell staining in RAW264.7, MLE-12 and HUVEC cells. Green, Calcein AM staining for live cells. Red, propidium iodide staining for dead cells (n = 3). (e) Cell skeleton staining in HUVECs. Green, FITC phalloidine. Blue, DAPI. (f) Blood routine and biochemical indexes ( n = 3). (g) Representative TUNEL staining of lung tissues from GRb1@LEVs-cRGD and control groups (n = 3). (h) Histopathological examination by H&E staining of major organs (n = 3).

Article Snippet: Fluorescein phalloidin and cyanine5.5 amine were procured from MedChemExpress (USA).

Techniques: In Vitro, In Vivo, CCK-8 Assay, Staining, TUNEL Assay, Control

Clinoptilolite zeolite reduces LPS-induced epithelial permeability in Caco-2 monolayers. Caco-2 cells were cultured on 0.4-µm Transwell inserts for 7 days to allow epithelial monolayer formation prior to treatment with lipopolysaccharide (LPS), clinoptilolite zeolite (ZEO), or combined LPS + ZEO conditions for 24 h. Epithelial permeability was subsequently evaluated using FITC-dextran (70 kDa) translocation across the epithelial barrier. Data are presented as relative fluorescence units (RFU) ± SD. Statistical significance was determined using an unpaired Student’s t-test.

Journal: Frontiers in Immunology

Article Title: Adsorption-mediated modulation of lipopolysaccharide bioactivity by clinoptilolite zeolite with in vitro immunomodulatory effects and in vivo safety evaluation

doi: 10.3389/fimmu.2026.1818740

Figure Lengend Snippet: Clinoptilolite zeolite reduces LPS-induced epithelial permeability in Caco-2 monolayers. Caco-2 cells were cultured on 0.4-µm Transwell inserts for 7 days to allow epithelial monolayer formation prior to treatment with lipopolysaccharide (LPS), clinoptilolite zeolite (ZEO), or combined LPS + ZEO conditions for 24 h. Epithelial permeability was subsequently evaluated using FITC-dextran (70 kDa) translocation across the epithelial barrier. Data are presented as relative fluorescence units (RFU) ± SD. Statistical significance was determined using an unpaired Student’s t-test.

Article Snippet: Fluorescein isothiocyanate (FITC)-dextran (70 kDa; MedChemExpress, HY-128868E) dissolved in HBSS was added to the apical compartment at a final concentration of 250 μg/mL.

Techniques: Permeability, Cell Culture, Translocation Assay, Fluorescence

SOS1 inhibition attenuates extracellular matrix deposition, stellate cell activation, and downstream signaling in LX2 hepatic stellate cells (A–D) Decellularized extracellular matrix (ECM) derived from activated LX2 cells treated with increasing concentrations of SOS1 inhibitor (SOS-I) and stained with NHS-Fluorescein, showing a progressive reduction in ECM deposition with SOS1 inhibition. (E) Representative immunoblot of fibrogenic markers (COL1A1, FN1, α-SMA, PDGFRB) with calnexin as loading control, demonstrating reduced protein expression following SOS-I treatment. (F–I) Quantitative analyses of fibrogenic and inflammatory readouts showing modulation of ECM-associated and signaling markers following SOS1 inhibition. (J–M) Immunofluorescence staining of extracellular matrix components, including collagen (green, J and K) and fibronectin (red, L and M), demonstrating reduced matrix deposition in SOS-I-treated cells. Nuclei are counterstained with DAPI (blue). (N and O) BODIPY staining of LX2 cells showing increased lipid droplet accumulation following SOS1 inhibition, consistent with partial reversion of stellate cell activation. (P and Q) Transwell migration assays demonstrating reduced migratory capacity of activated LX2 cells following SOS-I treatment. (R) Immunoblot analysis of pERK and total ERK in LX2 cells stimulated with PDGFB in the presence or absence of SOS-I, with calnexin as loading control, showing attenuation of PDGFB-induced ERK phosphorylation. (S) Immunoblot analysis of pERK and total ERK in LX2 cells treated with increasing concentrations of SOS-I, demonstrating dose-dependent reduction in ERK phosphorylation. (T) qRT-PCR confirmation of siRNA-mediated SOS1 knockdown using two independent siRNAs (13.1 and 13.2), with expression normalized to GAPDH. (U) Immunoblot analysis showing the effect of SOS1 knockdown on COL1A1 and IL-1β protein expression, with calnexin as loading control. Data are presented as mean ± SEM with individual data points shown. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01. Statistical analyses were performed using one-way ANOVA with Tukey’s post hoc test or two-tailed unpaired Student’s t test where appropriate. Data represent mean ± SEM from n = 3 independent experiments (LX-2 studies). Exact p values are shown in the graphs. Scale bars, 400 μm for ECM imaging in (A–D); 200 μm for extracellular collagen and fibronectin immunofluorescence images (J–M) and BODIPY staining (N and O); and 100 μm for transwell migration assay images (P and Q).

Journal: iScience

Article Title: Serum SOS1 as a prognostic biomarker and therapeutic target for progressive liver disease

doi: 10.1016/j.isci.2026.116430

Figure Lengend Snippet: SOS1 inhibition attenuates extracellular matrix deposition, stellate cell activation, and downstream signaling in LX2 hepatic stellate cells (A–D) Decellularized extracellular matrix (ECM) derived from activated LX2 cells treated with increasing concentrations of SOS1 inhibitor (SOS-I) and stained with NHS-Fluorescein, showing a progressive reduction in ECM deposition with SOS1 inhibition. (E) Representative immunoblot of fibrogenic markers (COL1A1, FN1, α-SMA, PDGFRB) with calnexin as loading control, demonstrating reduced protein expression following SOS-I treatment. (F–I) Quantitative analyses of fibrogenic and inflammatory readouts showing modulation of ECM-associated and signaling markers following SOS1 inhibition. (J–M) Immunofluorescence staining of extracellular matrix components, including collagen (green, J and K) and fibronectin (red, L and M), demonstrating reduced matrix deposition in SOS-I-treated cells. Nuclei are counterstained with DAPI (blue). (N and O) BODIPY staining of LX2 cells showing increased lipid droplet accumulation following SOS1 inhibition, consistent with partial reversion of stellate cell activation. (P and Q) Transwell migration assays demonstrating reduced migratory capacity of activated LX2 cells following SOS-I treatment. (R) Immunoblot analysis of pERK and total ERK in LX2 cells stimulated with PDGFB in the presence or absence of SOS-I, with calnexin as loading control, showing attenuation of PDGFB-induced ERK phosphorylation. (S) Immunoblot analysis of pERK and total ERK in LX2 cells treated with increasing concentrations of SOS-I, demonstrating dose-dependent reduction in ERK phosphorylation. (T) qRT-PCR confirmation of siRNA-mediated SOS1 knockdown using two independent siRNAs (13.1 and 13.2), with expression normalized to GAPDH. (U) Immunoblot analysis showing the effect of SOS1 knockdown on COL1A1 and IL-1β protein expression, with calnexin as loading control. Data are presented as mean ± SEM with individual data points shown. Statistical significance is indicated as ∗ p < 0.05, ∗∗ p < 0.01. Statistical analyses were performed using one-way ANOVA with Tukey’s post hoc test or two-tailed unpaired Student’s t test where appropriate. Data represent mean ± SEM from n = 3 independent experiments (LX-2 studies). Exact p values are shown in the graphs. Scale bars, 400 μm for ECM imaging in (A–D); 200 μm for extracellular collagen and fibronectin immunofluorescence images (J–M) and BODIPY staining (N and O); and 100 μm for transwell migration assay images (P and Q).

Article Snippet: NHS-Fluorescein , ThermoFisher , Catalog # 46409.

Techniques: Inhibition, Activation Assay, Derivative Assay, Staining, Western Blot, Control, Expressing, Immunofluorescence, Migration, Phospho-proteomics, Quantitative RT-PCR, Knockdown, Two Tailed Test, Imaging, Transwell Migration Assay