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rabbit anti rat collagen type iii polyclonal antibody  (Bio-Rad)


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    Bio-Rad rabbit anti rat collagen type iii polyclonal antibody
    Rabbit Anti Rat Collagen Type Iii Polyclonal Antibody, supplied by Bio-Rad, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti rat collagen type iii polyclonal antibody/product/Bio-Rad
    Average 93 stars, based on 11 article reviews
    rabbit anti rat collagen type iii polyclonal antibody - by Bioz Stars, 2026-03
    93/100 stars

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    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers <t>(COL</t> I, COL <t>III,</t> α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.
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    Image Search Results


    Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers (COL I, COL III, α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.

    Journal: International Journal of Nanomedicine

    Article Title: Antioxidant Carbon Dots and Ursolic Acid Co-Encapsulated Liposomes Composite Hydrogel for Alleviating Adhesion Formation and Enhancing Tendon Healing in Tendon Injury

    doi: 10.2147/ijn.s466312

    Figure Lengend Snippet: Figure 4 RCDs/UA@Lipo alleviated H2O2-induced oxidative stress and TGF-β1 induced fibrosis-specific markers separately. (A) Immunofluorescence staining images of intracellular ROS and superoxide detected by DCFH-DA probe. (B) mitochondrial membrane potential (ΔΨm) detected by JC-1 probe. (C) tendon fibrosis markers (COL I, COL III, α-SMA) of NIH3T3. (D–H) Semiquantitative analysis of the relative fluorescent intensity of (A–C) (n = 3). (D and E) Model group is H2O2 group, (F–H) Model group is TGF-β1 group. Data are presented as mean ± SD; comparisons between the groups were performed one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001.

    Article Snippet: Evaluation of Anti-Fibrotic Effects of the Biomaterials by Immunofluorescent Staining at Six Weeks The fresh tissue sections were incubated with rabbit anti-rat antibodies against COL III (1:200; Cat#22734-1-AP, Proteintech, USA) and α-SMA (1:200; Cat#19245S, Cell Signaling Technology, USA) at 4°C overnight.

    Techniques: Immunofluorescence, Staining, Membrane

    Figure 6 RCDs/UA@Lipo-HAMA reduced adhesion of injured tendons at macroscopic and histological levels at various time points post-injury. (A) Schematic diagram of surgical procedures of the ATI. (B) Gross view of ATI. (C)Representative images of immunofluorescence staining of tendon antioxidant (Nrf-2, HO-1) and anti-inflammatory markers (CD68, iNOS) at 2 weeks post-injury (n = 3). (D) Representative images of immunofluorescence staining of tendon antifibrosis (COL III, α-SMA) at 6 weeks post- injury (n = 3). (E) Representative images of immunohistochemical staining of tendon markers (Vimentin, MMP2, α-SMA) antifibrosis at 6 weeks post-injury (n = 4). (F–N) Semiquantitative analysis of expression level of tendon marker of (C–E), respectively. Data are presented as mean ± SD; comparisons between the groups were performed by one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Journal: International Journal of Nanomedicine

    Article Title: Antioxidant Carbon Dots and Ursolic Acid Co-Encapsulated Liposomes Composite Hydrogel for Alleviating Adhesion Formation and Enhancing Tendon Healing in Tendon Injury

    doi: 10.2147/ijn.s466312

    Figure Lengend Snippet: Figure 6 RCDs/UA@Lipo-HAMA reduced adhesion of injured tendons at macroscopic and histological levels at various time points post-injury. (A) Schematic diagram of surgical procedures of the ATI. (B) Gross view of ATI. (C)Representative images of immunofluorescence staining of tendon antioxidant (Nrf-2, HO-1) and anti-inflammatory markers (CD68, iNOS) at 2 weeks post-injury (n = 3). (D) Representative images of immunofluorescence staining of tendon antifibrosis (COL III, α-SMA) at 6 weeks post- injury (n = 3). (E) Representative images of immunohistochemical staining of tendon markers (Vimentin, MMP2, α-SMA) antifibrosis at 6 weeks post-injury (n = 4). (F–N) Semiquantitative analysis of expression level of tendon marker of (C–E), respectively. Data are presented as mean ± SD; comparisons between the groups were performed by one-way ANOVA. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Article Snippet: Evaluation of Anti-Fibrotic Effects of the Biomaterials by Immunofluorescent Staining at Six Weeks The fresh tissue sections were incubated with rabbit anti-rat antibodies against COL III (1:200; Cat#22734-1-AP, Proteintech, USA) and α-SMA (1:200; Cat#19245S, Cell Signaling Technology, USA) at 4°C overnight.

    Techniques: Immunofluorescence, Staining, Immunohistochemical staining, Expressing, Marker