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dio labeled pl720  (Beyotime)


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    Beyotime dio labeled pl720
    Figure 1. Schematic illustration of <t>PL720</t> cascade targeted therapy for MI/R in mice. When PL720 is administered at ischemia- reperfusion phase, it effectively targets the site of injury. Upon reaching the lesion site, the encapsulated L-arginine is released to facilitate the production of NO for timely vasodilation. Simultaneously, the slow-released FTY720 within the injured myocardium activates the AKT pathway in cardiomyocytes to alleviate cardiomyocyte apoptosis. When administered at the late perfusion inflammation phase, the PL720 captured monocyte (monocyte-PL720 aggregates) is recruited to the heart lesion. Recruited monocytes in the heart differentiate into macrophages, and subsequently, the macrophages phagocytize PL720. With the sustained release of FTY720, the STAT3 signaling pathway of macrophages is activated, thereby promoting macrophage polarization. This process reduces sprouting vessel degeneration caused by long M1 subtype macrophages while increasing M2 subtype macrophages to promote the maturation and quiescence of sprouting vessels.
    Dio Labeled Pl720, supplied by Beyotime, used in various techniques. Bioz Stars score: 99/100, based on 941 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/dio+labeled+pl720/pm38345237-341-11-31?v=Beyotime
    Average 99 stars, based on 941 article reviews
    dio labeled pl720 - by Bioz Stars, 2026-07
    99/100 stars

    Images

    1) Product Images from "Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury."

    Article Title: Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    doi: 10.1002/advs.202308727

    Figure 1. Schematic illustration of PL720 cascade targeted therapy for MI/R in mice. When PL720 is administered at ischemia- reperfusion phase, it effectively targets the site of injury. Upon reaching the lesion site, the encapsulated L-arginine is released to facilitate the production of NO for timely vasodilation. Simultaneously, the slow-released FTY720 within the injured myocardium activates the AKT pathway in cardiomyocytes to alleviate cardiomyocyte apoptosis. When administered at the late perfusion inflammation phase, the PL720 captured monocyte (monocyte-PL720 aggregates) is recruited to the heart lesion. Recruited monocytes in the heart differentiate into macrophages, and subsequently, the macrophages phagocytize PL720. With the sustained release of FTY720, the STAT3 signaling pathway of macrophages is activated, thereby promoting macrophage polarization. This process reduces sprouting vessel degeneration caused by long M1 subtype macrophages while increasing M2 subtype macrophages to promote the maturation and quiescence of sprouting vessels.
    Figure Legend Snippet: Figure 1. Schematic illustration of PL720 cascade targeted therapy for MI/R in mice. When PL720 is administered at ischemia- reperfusion phase, it effectively targets the site of injury. Upon reaching the lesion site, the encapsulated L-arginine is released to facilitate the production of NO for timely vasodilation. Simultaneously, the slow-released FTY720 within the injured myocardium activates the AKT pathway in cardiomyocytes to alleviate cardiomyocyte apoptosis. When administered at the late perfusion inflammation phase, the PL720 captured monocyte (monocyte-PL720 aggregates) is recruited to the heart lesion. Recruited monocytes in the heart differentiate into macrophages, and subsequently, the macrophages phagocytize PL720. With the sustained release of FTY720, the STAT3 signaling pathway of macrophages is activated, thereby promoting macrophage polarization. This process reduces sprouting vessel degeneration caused by long M1 subtype macrophages while increasing M2 subtype macrophages to promote the maturation and quiescence of sprouting vessels.

    Techniques Used:

    Figure 2. Preparation and characterization of PL720. a) Schematic diagram of PL720 fabrication. b) TEM image of PNVs and PL720. c) Mean diameter of PLTs, PNVs, and PL720 (n = 5). d) Zeta potential (𝜉) analysis of PLTs, PNVs, and PL720 (n = 5). e) Polymer dispersity index (PDI) of PLTs, PMVs, and PL720 (n = 3). f. Release profiles of L-arginine and FTY720 from PL720 within 24 h. g) Quantification of proteins in PLTs, purified platelet membrane, and PL720 identified by LC-MS/MS. The Venn diagram illustrates the protein overlap among PLTs, purified platelet membrane, and PL720. h) Volcano plot displaying differential proteins between purified platelet membrane and PL720. The red points indicate significantly up-regulated proteins. The blue points represent significantly down-regulated proteins (n = 3; fold change > 2 and adj. Pval < 0.05); and the gray points represent proteins without significant differential changes. i) Expression abundance of proteins associated with platelet adhesion and immune escape properties in purified platelet membrane and PL720 (n = 3). j) Classification of PL720 proteins by molecular function. k) Classification of PL720 Proteins by biological process. Results are presented as mean ± SD.
    Figure Legend Snippet: Figure 2. Preparation and characterization of PL720. a) Schematic diagram of PL720 fabrication. b) TEM image of PNVs and PL720. c) Mean diameter of PLTs, PNVs, and PL720 (n = 5). d) Zeta potential (𝜉) analysis of PLTs, PNVs, and PL720 (n = 5). e) Polymer dispersity index (PDI) of PLTs, PMVs, and PL720 (n = 3). f. Release profiles of L-arginine and FTY720 from PL720 within 24 h. g) Quantification of proteins in PLTs, purified platelet membrane, and PL720 identified by LC-MS/MS. The Venn diagram illustrates the protein overlap among PLTs, purified platelet membrane, and PL720. h) Volcano plot displaying differential proteins between purified platelet membrane and PL720. The red points indicate significantly up-regulated proteins. The blue points represent significantly down-regulated proteins (n = 3; fold change > 2 and adj. Pval < 0.05); and the gray points represent proteins without significant differential changes. i) Expression abundance of proteins associated with platelet adhesion and immune escape properties in purified platelet membrane and PL720 (n = 3). j) Classification of PL720 proteins by molecular function. k) Classification of PL720 Proteins by biological process. Results are presented as mean ± SD.

    Techniques Used: Zeta Potential Analyzer, Polymer, Membrane, Liquid Chromatography with Mass Spectroscopy, Expressing

    Figure 3. In vitro assessment of the anti-apoptotic and NO-generating capacity of PL720. a) CLSM images of HUVECs stained with DAF-FM DA after interacting with PL720 at predetermined time points. b) Quantitative analysis of the mean fluorescence intensity of HUVECs in (a) (n = 3). c) Relative nitrite levels in the culture supernatants of HUVECs using the Griess reaction (n = 3). d) Evaluation of the anti-apoptotic effects of PBS, PNVs, FTY720, L-arginine, and PL720 on H/R-treated H9C2 cardiomyocytes. e) Quantitative analysis of apoptosis percentage of H9C2 cells in (d) (n = 3). f) WB analysis of p-AKT, AKT, BAX, and BCL-2 protein levels. g) Quantitative analysis of p-AKT/AKT levels in (f) (n = 3). h) Quantitative analysis of BAX/BCL-2 levels (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.
    Figure Legend Snippet: Figure 3. In vitro assessment of the anti-apoptotic and NO-generating capacity of PL720. a) CLSM images of HUVECs stained with DAF-FM DA after interacting with PL720 at predetermined time points. b) Quantitative analysis of the mean fluorescence intensity of HUVECs in (a) (n = 3). c) Relative nitrite levels in the culture supernatants of HUVECs using the Griess reaction (n = 3). d) Evaluation of the anti-apoptotic effects of PBS, PNVs, FTY720, L-arginine, and PL720 on H/R-treated H9C2 cardiomyocytes. e) Quantitative analysis of apoptosis percentage of H9C2 cells in (d) (n = 3). f) WB analysis of p-AKT, AKT, BAX, and BCL-2 protein levels. g) Quantitative analysis of p-AKT/AKT levels in (f) (n = 3). h) Quantitative analysis of BAX/BCL-2 levels (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Techniques Used: In Vitro, Staining, Two Tailed Test

    Figure 4. In vitro monocyte-binding ability and macrophage uptake ability of PL720. a) Representative CLSM images of THP-1 monocytes bound with DiO-labeled PL720 and anti-CD62P antibody blocked PL720 after pre-incubation with or without LPS+INF-𝛾stimulation (red: cell membrane, green: PL720, blue: nuclei). b) Semi-quantification of DiO fluorescence intensity in (a) (n = 4). c) Flow cytometry analysis of THP-1 monocytes bound with DiO-labeled PL720 and PL720 62Pblock after pre-incubation with or without inflammatory activation. d) Quantification of DiO normalized fluorescence intensity in (c) (n = 3). e) Representative CLSM images of monocytes (THP-1) and macrophages (THP-1 (MΦ)) after incubation with DiO-labeled PL720
    Figure Legend Snippet: Figure 4. In vitro monocyte-binding ability and macrophage uptake ability of PL720. a) Representative CLSM images of THP-1 monocytes bound with DiO-labeled PL720 and anti-CD62P antibody blocked PL720 after pre-incubation with or without LPS+INF-𝛾stimulation (red: cell membrane, green: PL720, blue: nuclei). b) Semi-quantification of DiO fluorescence intensity in (a) (n = 4). c) Flow cytometry analysis of THP-1 monocytes bound with DiO-labeled PL720 and PL720 62Pblock after pre-incubation with or without inflammatory activation. d) Quantification of DiO normalized fluorescence intensity in (c) (n = 3). e) Representative CLSM images of monocytes (THP-1) and macrophages (THP-1 (MΦ)) after incubation with DiO-labeled PL720

    Techniques Used: In Vitro, Binding Assay, Labeling, Incubation, Membrane, Flow Cytometry, Activation Assay

    Figure 5. PL720 activates STAT3 pathway to induce immunomodulation in vitro. a) CLSM images indicate phenotypes of inflammatory BMDMs after being treated by PBS, FTY720, and PL720. b) Quantitative analysis of fluorescence intensity of iNOS (M1) and CD206 (M2) in (a) (n = 3). c) Flow cytometry assay of inflammatory BMDMs after treated by PBS, FTY720, and PL720. d) Statistical analysis of flow cytometry results in (c) (n = 3). e) WB of p-STAT3, STAT3, INOS, and CD206 protein. f–h). Quantification of p-STAT3/STAT3, INOS/GAPDH and CD206/GAPDH levels (n = 3). i–k) Concentration of cytokine M1 markers (IL-1𝛽, TNF-𝛼) and M2 markers (IL-10, TGF-𝛽) in supernatants (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.
    Figure Legend Snippet: Figure 5. PL720 activates STAT3 pathway to induce immunomodulation in vitro. a) CLSM images indicate phenotypes of inflammatory BMDMs after being treated by PBS, FTY720, and PL720. b) Quantitative analysis of fluorescence intensity of iNOS (M1) and CD206 (M2) in (a) (n = 3). c) Flow cytometry assay of inflammatory BMDMs after treated by PBS, FTY720, and PL720. d) Statistical analysis of flow cytometry results in (c) (n = 3). e) WB of p-STAT3, STAT3, INOS, and CD206 protein. f–h). Quantification of p-STAT3/STAT3, INOS/GAPDH and CD206/GAPDH levels (n = 3). i–k) Concentration of cytokine M1 markers (IL-1𝛽, TNF-𝛼) and M2 markers (IL-10, TGF-𝛽) in supernatants (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Techniques Used: In Vitro, Flow Cytometry, Cytometry, Concentration Assay, Two Tailed Test

    Figure 7. Targeting specificity, and macrophage polarization reprogramming effect of a single dose of PL720 during the late reperfusion inflammation phase. a) The typical ex vivo NIR images of the heart for sham group or MI/R mice injected with DiR-labeled PL720 or PL720 62Pblock. b) Quantitative analysis of DiR fluorescence signal in hearts for different groups of mice (n = 3). c) The CLSM image of the injury site in the heart after injection of DiI-labeled PL720 and PL720 62Pblock. d) Quantitative analysis of DiI fluorescence signal in hearts for different groups of mice (n = 3). e) CLSM images of MI/R injured heart sections showing the total (F4/80) and M2 subtype (CD206) macrophages after being treated by PBS, PNVs, L720, and PL720, respectively. f) Fluorescence intensity quantification of F4/80 in (e) (n = 4). g) Fluorescence intensity quantification of CD206 in (e) (n = 4). h) WB of p-STAT3, STAT3, INOS, and CD206 protein levels. i–k) Quantification of p-STAT3/STAT3, INOS/GAPDH and CD206/GAPDH levels (n = 3). l–o) Quantification of L-1𝛽, TNF-𝛼, IL-10, and TGF-𝛽related mRNA expression (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.
    Figure Legend Snippet: Figure 7. Targeting specificity, and macrophage polarization reprogramming effect of a single dose of PL720 during the late reperfusion inflammation phase. a) The typical ex vivo NIR images of the heart for sham group or MI/R mice injected with DiR-labeled PL720 or PL720 62Pblock. b) Quantitative analysis of DiR fluorescence signal in hearts for different groups of mice (n = 3). c) The CLSM image of the injury site in the heart after injection of DiI-labeled PL720 and PL720 62Pblock. d) Quantitative analysis of DiI fluorescence signal in hearts for different groups of mice (n = 3). e) CLSM images of MI/R injured heart sections showing the total (F4/80) and M2 subtype (CD206) macrophages after being treated by PBS, PNVs, L720, and PL720, respectively. f) Fluorescence intensity quantification of F4/80 in (e) (n = 4). g) Fluorescence intensity quantification of CD206 in (e) (n = 4). h) WB of p-STAT3, STAT3, INOS, and CD206 protein levels. i–k) Quantification of p-STAT3/STAT3, INOS/GAPDH and CD206/GAPDH levels (n = 3). l–o) Quantification of L-1𝛽, TNF-𝛼, IL-10, and TGF-𝛽related mRNA expression (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Techniques Used: Ex Vivo, Injection, Labeling, Fluorescence, Expressing, Two Tailed Test

    Figure 8. Cardioprotection effect after two doses of PL720 treatment. a) Echocardiograms obtained by M-mode ultrasound at different times post- operation (pre, day 3, day 7, and day 28). b–g) Cardiac function of the mice was evaluated according to the EF, FS, LVID; d, LV Vol; d, LVID; s and LV
    Figure Legend Snippet: Figure 8. Cardioprotection effect after two doses of PL720 treatment. a) Echocardiograms obtained by M-mode ultrasound at different times post- operation (pre, day 3, day 7, and day 28). b–g) Cardiac function of the mice was evaluated according to the EF, FS, LVID; d, LV Vol; d, LVID; s and LV

    Techniques Used:



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    dio labeled pl720  (Beyotime)
    99
    Beyotime dio labeled pl720
    Figure 1. Schematic illustration of <t>PL720</t> cascade targeted therapy for MI/R in mice. When PL720 is administered at ischemia- reperfusion phase, it effectively targets the site of injury. Upon reaching the lesion site, the encapsulated L-arginine is released to facilitate the production of NO for timely vasodilation. Simultaneously, the slow-released FTY720 within the injured myocardium activates the AKT pathway in cardiomyocytes to alleviate cardiomyocyte apoptosis. When administered at the late perfusion inflammation phase, the PL720 captured monocyte (monocyte-PL720 aggregates) is recruited to the heart lesion. Recruited monocytes in the heart differentiate into macrophages, and subsequently, the macrophages phagocytize PL720. With the sustained release of FTY720, the STAT3 signaling pathway of macrophages is activated, thereby promoting macrophage polarization. This process reduces sprouting vessel degeneration caused by long M1 subtype macrophages while increasing M2 subtype macrophages to promote the maturation and quiescence of sprouting vessels.
    Dio Labeled Pl720, supplied by Beyotime, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/dio+labeled+pl720/pm38345237-341-11-31?v=Beyotime
    Average 99 stars, based on 1 article reviews
    dio labeled pl720 - by Bioz Stars, 2026-07
    99/100 stars
    		  Buy from Supplier

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    Figure 1. Schematic illustration of PL720 cascade targeted therapy for MI/R in mice. When PL720 is administered at ischemia- reperfusion phase, it effectively targets the site of injury. Upon reaching the lesion site, the encapsulated L-arginine is released to facilitate the production of NO for timely vasodilation. Simultaneously, the slow-released FTY720 within the injured myocardium activates the AKT pathway in cardiomyocytes to alleviate cardiomyocyte apoptosis. When administered at the late perfusion inflammation phase, the PL720 captured monocyte (monocyte-PL720 aggregates) is recruited to the heart lesion. Recruited monocytes in the heart differentiate into macrophages, and subsequently, the macrophages phagocytize PL720. With the sustained release of FTY720, the STAT3 signaling pathway of macrophages is activated, thereby promoting macrophage polarization. This process reduces sprouting vessel degeneration caused by long M1 subtype macrophages while increasing M2 subtype macrophages to promote the maturation and quiescence of sprouting vessels.

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.

    doi: 10.1002/advs.202308727

    Figure Lengend Snippet: Figure 1. Schematic illustration of PL720 cascade targeted therapy for MI/R in mice. When PL720 is administered at ischemia- reperfusion phase, it effectively targets the site of injury. Upon reaching the lesion site, the encapsulated L-arginine is released to facilitate the production of NO for timely vasodilation. Simultaneously, the slow-released FTY720 within the injured myocardium activates the AKT pathway in cardiomyocytes to alleviate cardiomyocyte apoptosis. When administered at the late perfusion inflammation phase, the PL720 captured monocyte (monocyte-PL720 aggregates) is recruited to the heart lesion. Recruited monocytes in the heart differentiate into macrophages, and subsequently, the macrophages phagocytize PL720. With the sustained release of FTY720, the STAT3 signaling pathway of macrophages is activated, thereby promoting macrophage polarization. This process reduces sprouting vessel degeneration caused by long M1 subtype macrophages while increasing M2 subtype macrophages to promote the maturation and quiescence of sprouting vessels.

    Article Snippet: Both inflammatory and non-inflammatory activated THP-1 cells were incubated with green DiO-labeled PL720 or CD-62P-inhibited PL720 for 60 min. THP-1 cells were stained using a DiI (red) cell membrane staining kit (Beyotime, China) and observed using CLSM.

    Techniques:

    Figure 2. Preparation and characterization of PL720. a) Schematic diagram of PL720 fabrication. b) TEM image of PNVs and PL720. c) Mean diameter of PLTs, PNVs, and PL720 (n = 5). d) Zeta potential (𝜉) analysis of PLTs, PNVs, and PL720 (n = 5). e) Polymer dispersity index (PDI) of PLTs, PMVs, and PL720 (n = 3). f. Release profiles of L-arginine and FTY720 from PL720 within 24 h. g) Quantification of proteins in PLTs, purified platelet membrane, and PL720 identified by LC-MS/MS. The Venn diagram illustrates the protein overlap among PLTs, purified platelet membrane, and PL720. h) Volcano plot displaying differential proteins between purified platelet membrane and PL720. The red points indicate significantly up-regulated proteins. The blue points represent significantly down-regulated proteins (n = 3; fold change > 2 and adj. Pval < 0.05); and the gray points represent proteins without significant differential changes. i) Expression abundance of proteins associated with platelet adhesion and immune escape properties in purified platelet membrane and PL720 (n = 3). j) Classification of PL720 proteins by molecular function. k) Classification of PL720 Proteins by biological process. Results are presented as mean ± SD.

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.

    doi: 10.1002/advs.202308727

    Figure Lengend Snippet: Figure 2. Preparation and characterization of PL720. a) Schematic diagram of PL720 fabrication. b) TEM image of PNVs and PL720. c) Mean diameter of PLTs, PNVs, and PL720 (n = 5). d) Zeta potential (𝜉) analysis of PLTs, PNVs, and PL720 (n = 5). e) Polymer dispersity index (PDI) of PLTs, PMVs, and PL720 (n = 3). f. Release profiles of L-arginine and FTY720 from PL720 within 24 h. g) Quantification of proteins in PLTs, purified platelet membrane, and PL720 identified by LC-MS/MS. The Venn diagram illustrates the protein overlap among PLTs, purified platelet membrane, and PL720. h) Volcano plot displaying differential proteins between purified platelet membrane and PL720. The red points indicate significantly up-regulated proteins. The blue points represent significantly down-regulated proteins (n = 3; fold change > 2 and adj. Pval < 0.05); and the gray points represent proteins without significant differential changes. i) Expression abundance of proteins associated with platelet adhesion and immune escape properties in purified platelet membrane and PL720 (n = 3). j) Classification of PL720 proteins by molecular function. k) Classification of PL720 Proteins by biological process. Results are presented as mean ± SD.

    Article Snippet: Both inflammatory and non-inflammatory activated THP-1 cells were incubated with green DiO-labeled PL720 or CD-62P-inhibited PL720 for 60 min. THP-1 cells were stained using a DiI (red) cell membrane staining kit (Beyotime, China) and observed using CLSM.

    Techniques: Zeta Potential Analyzer, Polymer, Membrane, Liquid Chromatography with Mass Spectroscopy, Expressing

    Figure 3. In vitro assessment of the anti-apoptotic and NO-generating capacity of PL720. a) CLSM images of HUVECs stained with DAF-FM DA after interacting with PL720 at predetermined time points. b) Quantitative analysis of the mean fluorescence intensity of HUVECs in (a) (n = 3). c) Relative nitrite levels in the culture supernatants of HUVECs using the Griess reaction (n = 3). d) Evaluation of the anti-apoptotic effects of PBS, PNVs, FTY720, L-arginine, and PL720 on H/R-treated H9C2 cardiomyocytes. e) Quantitative analysis of apoptosis percentage of H9C2 cells in (d) (n = 3). f) WB analysis of p-AKT, AKT, BAX, and BCL-2 protein levels. g) Quantitative analysis of p-AKT/AKT levels in (f) (n = 3). h) Quantitative analysis of BAX/BCL-2 levels (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.

    doi: 10.1002/advs.202308727

    Figure Lengend Snippet: Figure 3. In vitro assessment of the anti-apoptotic and NO-generating capacity of PL720. a) CLSM images of HUVECs stained with DAF-FM DA after interacting with PL720 at predetermined time points. b) Quantitative analysis of the mean fluorescence intensity of HUVECs in (a) (n = 3). c) Relative nitrite levels in the culture supernatants of HUVECs using the Griess reaction (n = 3). d) Evaluation of the anti-apoptotic effects of PBS, PNVs, FTY720, L-arginine, and PL720 on H/R-treated H9C2 cardiomyocytes. e) Quantitative analysis of apoptosis percentage of H9C2 cells in (d) (n = 3). f) WB analysis of p-AKT, AKT, BAX, and BCL-2 protein levels. g) Quantitative analysis of p-AKT/AKT levels in (f) (n = 3). h) Quantitative analysis of BAX/BCL-2 levels (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Article Snippet: Both inflammatory and non-inflammatory activated THP-1 cells were incubated with green DiO-labeled PL720 or CD-62P-inhibited PL720 for 60 min. THP-1 cells were stained using a DiI (red) cell membrane staining kit (Beyotime, China) and observed using CLSM.

    Techniques: In Vitro, Staining, Two Tailed Test

    Figure 4. In vitro monocyte-binding ability and macrophage uptake ability of PL720. a) Representative CLSM images of THP-1 monocytes bound with DiO-labeled PL720 and anti-CD62P antibody blocked PL720 after pre-incubation with or without LPS+INF-𝛾stimulation (red: cell membrane, green: PL720, blue: nuclei). b) Semi-quantification of DiO fluorescence intensity in (a) (n = 4). c) Flow cytometry analysis of THP-1 monocytes bound with DiO-labeled PL720 and PL720 62Pblock after pre-incubation with or without inflammatory activation. d) Quantification of DiO normalized fluorescence intensity in (c) (n = 3). e) Representative CLSM images of monocytes (THP-1) and macrophages (THP-1 (MΦ)) after incubation with DiO-labeled PL720

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.

    doi: 10.1002/advs.202308727

    Figure Lengend Snippet: Figure 4. In vitro monocyte-binding ability and macrophage uptake ability of PL720. a) Representative CLSM images of THP-1 monocytes bound with DiO-labeled PL720 and anti-CD62P antibody blocked PL720 after pre-incubation with or without LPS+INF-𝛾stimulation (red: cell membrane, green: PL720, blue: nuclei). b) Semi-quantification of DiO fluorescence intensity in (a) (n = 4). c) Flow cytometry analysis of THP-1 monocytes bound with DiO-labeled PL720 and PL720 62Pblock after pre-incubation with or without inflammatory activation. d) Quantification of DiO normalized fluorescence intensity in (c) (n = 3). e) Representative CLSM images of monocytes (THP-1) and macrophages (THP-1 (MΦ)) after incubation with DiO-labeled PL720

    Article Snippet: Both inflammatory and non-inflammatory activated THP-1 cells were incubated with green DiO-labeled PL720 or CD-62P-inhibited PL720 for 60 min. THP-1 cells were stained using a DiI (red) cell membrane staining kit (Beyotime, China) and observed using CLSM.

    Techniques: In Vitro, Binding Assay, Labeling, Incubation, Membrane, Flow Cytometry, Activation Assay

    Figure 5. PL720 activates STAT3 pathway to induce immunomodulation in vitro. a) CLSM images indicate phenotypes of inflammatory BMDMs after being treated by PBS, FTY720, and PL720. b) Quantitative analysis of fluorescence intensity of iNOS (M1) and CD206 (M2) in (a) (n = 3). c) Flow cytometry assay of inflammatory BMDMs after treated by PBS, FTY720, and PL720. d) Statistical analysis of flow cytometry results in (c) (n = 3). e) WB of p-STAT3, STAT3, INOS, and CD206 protein. f–h). Quantification of p-STAT3/STAT3, INOS/GAPDH and CD206/GAPDH levels (n = 3). i–k) Concentration of cytokine M1 markers (IL-1𝛽, TNF-𝛼) and M2 markers (IL-10, TGF-𝛽) in supernatants (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.

    doi: 10.1002/advs.202308727

    Figure Lengend Snippet: Figure 5. PL720 activates STAT3 pathway to induce immunomodulation in vitro. a) CLSM images indicate phenotypes of inflammatory BMDMs after being treated by PBS, FTY720, and PL720. b) Quantitative analysis of fluorescence intensity of iNOS (M1) and CD206 (M2) in (a) (n = 3). c) Flow cytometry assay of inflammatory BMDMs after treated by PBS, FTY720, and PL720. d) Statistical analysis of flow cytometry results in (c) (n = 3). e) WB of p-STAT3, STAT3, INOS, and CD206 protein. f–h). Quantification of p-STAT3/STAT3, INOS/GAPDH and CD206/GAPDH levels (n = 3). i–k) Concentration of cytokine M1 markers (IL-1𝛽, TNF-𝛼) and M2 markers (IL-10, TGF-𝛽) in supernatants (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Article Snippet: Both inflammatory and non-inflammatory activated THP-1 cells were incubated with green DiO-labeled PL720 or CD-62P-inhibited PL720 for 60 min. THP-1 cells were stained using a DiI (red) cell membrane staining kit (Beyotime, China) and observed using CLSM.

    Techniques: In Vitro, Flow Cytometry, Cytometry, Concentration Assay, Two Tailed Test

    Figure 7. Targeting specificity, and macrophage polarization reprogramming effect of a single dose of PL720 during the late reperfusion inflammation phase. a) The typical ex vivo NIR images of the heart for sham group or MI/R mice injected with DiR-labeled PL720 or PL720 62Pblock. b) Quantitative analysis of DiR fluorescence signal in hearts for different groups of mice (n = 3). c) The CLSM image of the injury site in the heart after injection of DiI-labeled PL720 and PL720 62Pblock. d) Quantitative analysis of DiI fluorescence signal in hearts for different groups of mice (n = 3). e) CLSM images of MI/R injured heart sections showing the total (F4/80) and M2 subtype (CD206) macrophages after being treated by PBS, PNVs, L720, and PL720, respectively. f) Fluorescence intensity quantification of F4/80 in (e) (n = 4). g) Fluorescence intensity quantification of CD206 in (e) (n = 4). h) WB of p-STAT3, STAT3, INOS, and CD206 protein levels. i–k) Quantification of p-STAT3/STAT3, INOS/GAPDH and CD206/GAPDH levels (n = 3). l–o) Quantification of L-1𝛽, TNF-𝛼, IL-10, and TGF-𝛽related mRNA expression (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.

    doi: 10.1002/advs.202308727

    Figure Lengend Snippet: Figure 7. Targeting specificity, and macrophage polarization reprogramming effect of a single dose of PL720 during the late reperfusion inflammation phase. a) The typical ex vivo NIR images of the heart for sham group or MI/R mice injected with DiR-labeled PL720 or PL720 62Pblock. b) Quantitative analysis of DiR fluorescence signal in hearts for different groups of mice (n = 3). c) The CLSM image of the injury site in the heart after injection of DiI-labeled PL720 and PL720 62Pblock. d) Quantitative analysis of DiI fluorescence signal in hearts for different groups of mice (n = 3). e) CLSM images of MI/R injured heart sections showing the total (F4/80) and M2 subtype (CD206) macrophages after being treated by PBS, PNVs, L720, and PL720, respectively. f) Fluorescence intensity quantification of F4/80 in (e) (n = 4). g) Fluorescence intensity quantification of CD206 in (e) (n = 4). h) WB of p-STAT3, STAT3, INOS, and CD206 protein levels. i–k) Quantification of p-STAT3/STAT3, INOS/GAPDH and CD206/GAPDH levels (n = 3). l–o) Quantification of L-1𝛽, TNF-𝛼, IL-10, and TGF-𝛽related mRNA expression (n = 3). Results are reported as mean ± SD. Data were analyzed using one-way ANOVA followed by a two-tailed Student’s t-test. ns indicates non-significant (p > 0.05). * p < 0.05, **p < 0.01, and ***p < 0.001.

    Article Snippet: Both inflammatory and non-inflammatory activated THP-1 cells were incubated with green DiO-labeled PL720 or CD-62P-inhibited PL720 for 60 min. THP-1 cells were stained using a DiI (red) cell membrane staining kit (Beyotime, China) and observed using CLSM.

    Techniques: Ex Vivo, Injection, Labeling, Fluorescence, Expressing, Two Tailed Test

    Figure 8. Cardioprotection effect after two doses of PL720 treatment. a) Echocardiograms obtained by M-mode ultrasound at different times post- operation (pre, day 3, day 7, and day 28). b–g) Cardiac function of the mice was evaluated according to the EF, FS, LVID; d, LV Vol; d, LVID; s and LV

    Journal: Advanced science (Weinheim, Baden-Wurttemberg, Germany)

    Article Title: Platelet Membrane Nanocarriers Cascade Targeting Delivery System to Improve Myocardial Remodeling Post Myocardial Ischemia-Reperfusion Injury.

    doi: 10.1002/advs.202308727

    Figure Lengend Snippet: Figure 8. Cardioprotection effect after two doses of PL720 treatment. a) Echocardiograms obtained by M-mode ultrasound at different times post- operation (pre, day 3, day 7, and day 28). b–g) Cardiac function of the mice was evaluated according to the EF, FS, LVID; d, LV Vol; d, LVID; s and LV

    Article Snippet: Both inflammatory and non-inflammatory activated THP-1 cells were incubated with green DiO-labeled PL720 or CD-62P-inhibited PL720 for 60 min. THP-1 cells were stained using a DiI (red) cell membrane staining kit (Beyotime, China) and observed using CLSM.

    Techniques: