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antibodies against α sma  (Novus Biologicals)


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    Structured Review

    Novus Biologicals antibodies against α sma
    Antibodies Against α Sma, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 41 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/%CE%B1+smooth+muscle+actin+sma+antibody/pm42021508-48-27-35?v=Novus+Biologicals
    Average 95 stars, based on 41 article reviews
    antibodies against α sma - by Bioz Stars, 2026-08
    95/100 stars

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    Proteintech α sma
    Efficacy of GelMA MAVP MPs in promoting nerve end interface self-resolution. ( A ) Schematic of the peripheral sciatic nerve ligation (p-SNL) model with four experimental groups (i.e., MAVP, VAN, vehicle, and control) ( B ) Immunofluorescence (IF) staining of p-VEGFR2 and YAP (indicating mechanotransduction signaling). ( C ) The positive area percentage of p-VEGFR2 (n = 6). ( D ) Percentage of YAP in nuclear/cytoplasm (n = 6). ( E ) IF staining of proliferation signal (Ki-67) and vessel signal (CD31) for p-SNL animal. ( F ) Quantification of Ki-67/CD31 co-localization area percentage (n = 6). ( G ) IF co-staining of Ki-67 and macrophage marker F4/80. ( H ) Quantification of Ki-67/F4/80 co-localization area percentage (n = 6). ( I ) IF staining of scar <t>marker</t> <t>α-SMA.</t> ( J ) Quantification <t>of</t> <t>α-SMA-positive</t> area percentage (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , D , F , H and J ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
    α Sma, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MedChemExpress anti α smooth muscle actin α sma antibody
    Efficacy of GelMA MAVP MPs in promoting nerve end interface self-resolution. ( A ) Schematic of the peripheral sciatic nerve ligation (p-SNL) model with four experimental groups (i.e., MAVP, VAN, vehicle, and control) ( B ) Immunofluorescence (IF) staining of p-VEGFR2 and YAP (indicating mechanotransduction signaling). ( C ) The positive area percentage of p-VEGFR2 (n = 6). ( D ) Percentage of YAP in nuclear/cytoplasm (n = 6). ( E ) IF staining of proliferation signal (Ki-67) and vessel signal (CD31) for p-SNL animal. ( F ) Quantification of Ki-67/CD31 co-localization area percentage (n = 6). ( G ) IF co-staining of Ki-67 and macrophage marker F4/80. ( H ) Quantification of Ki-67/F4/80 co-localization area percentage (n = 6). ( I ) IF staining of scar <t>marker</t> <t>α-SMA.</t> ( J ) Quantification <t>of</t> <t>α-SMA-positive</t> area percentage (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , D , F , H and J ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.
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    Proteintech α smooth muscle actin
    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; <t>α-SMA,</t> <t>α-smooth</t> muscle actin; Vim; vimentin; ns, not significant.
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    Novus Biologicals antibodies against α sma
    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; <t>α-SMA,</t> <t>α-smooth</t> muscle actin; Vim; vimentin; ns, not significant.
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    R&D Systems mouse anti α sma
    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; <t>α-SMA,</t> <t>α-smooth</t> muscle actin; Vim; vimentin; ns, not significant.
    Mouse Anti α Sma, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Wuhan Sanying Biotechnology antibodies against α smooth muscle actin α sma
    Effects of CoQ10 on fibrosis-related proteins in rat lung tissue induced by SiO 2 dust suspension. ( (A) Effect of CoQ10 on HYP content in rat lungs induced by silica dust; (B) Effect of CoQ10 on the expression of EMT-related proteins in rat lungs induced by silica dust; (C) E-cad protein expression level; (D) Vimentin protein expression level; <t>(E)</t> <t>α-SMA</t> protein expression level; (F) Immunohistochemical detection <t>of</t> <t>α-SMA</t> protein expression (10×); <t>(G)</t> <t>α-SMA</t> protein positive expression level; (H) Effect of CoQ10 on collagen protein expression in rat lung tissue induced by silica dust; (I) Collagen-I protein expression level; (J) Collagen-III protein expression level. Note: * indicates P < 0.05 compared with the Control group; ** indicates P < 0.01 compared with the Control group; # indicates P < 0.05 compared with the Silicosis Model group; ## indicates P < 0.01 compared with the Silicosis Model group. All data are presented as mean ± standard deviation (M ± SD), n = 3).
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    Novus Biologicals mouse monoclonal anti α smooth muscle actin α sma
    Histopathologic evaluation of ulcer healing. a Thickness of granulation tissue and representative images of Azan-Mallory staining in the rebamipide and control groups on POD 7 (Scale bar, 1000 µm). The rebamipide group exhibited a greater thickness of granulation tissue compared with the control group (718.0 ± 144.0 µm vs. 589.6 ± 84.9 µm), although this difference did not reach statistical significance (P = 0.12). b The number of microvessels and representative images <t>of</t> <t>α-SMA</t> sections in the rebamipide and control groups on POD 7 (Scale bar, 50 µm). Although the rebamipide group showed a greater number of microvessels (17.0 ± 3.4 vs. 13.8 ± 1.5), the difference was not statistically significant (P = 0.10). c Widths of absent muscularis mucosae and representative images of Azan Mallory staining in the rebamipide and control groups on PODs 7, 14 and 21 (Scale bar, 2500 µm for POD 7; 1000 µm for PODs 14 and 21). Mean widths in the rebamipide and control groups on PODs 7, 14, and 21 were 13.8 ± 2.8 ×10³/µm vs. 13.9 ± 2.2 ×10³/µm (P = 0.93), 4.0 ± 1.7 ×10³/µm vs. 5.3 ± 1.9 ×10³/µm (P = 0.33), and 2.3 ± 1.6 ×10³/µm vs. 3.5 ± 2.2 ×10³/µm (P = 0.37), respectively. Although widths tended to be shorter in the rebamipide group on PODs 14 and 21, no statistically significant differences were detected. Linear mixed‑effects analysis revealed no significant group-time interaction. α-SMA, α-smooth muscle actin; POD, postoperative day.
    Mouse Monoclonal Anti α Smooth Muscle Actin α Sma, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    R&D Systems nti α sma apc
    Histopathologic evaluation of ulcer healing. a Thickness of granulation tissue and representative images of Azan-Mallory staining in the rebamipide and control groups on POD 7 (Scale bar, 1000 µm). The rebamipide group exhibited a greater thickness of granulation tissue compared with the control group (718.0 ± 144.0 µm vs. 589.6 ± 84.9 µm), although this difference did not reach statistical significance (P = 0.12). b The number of microvessels and representative images <t>of</t> <t>α-SMA</t> sections in the rebamipide and control groups on POD 7 (Scale bar, 50 µm). Although the rebamipide group showed a greater number of microvessels (17.0 ± 3.4 vs. 13.8 ± 1.5), the difference was not statistically significant (P = 0.10). c Widths of absent muscularis mucosae and representative images of Azan Mallory staining in the rebamipide and control groups on PODs 7, 14 and 21 (Scale bar, 2500 µm for POD 7; 1000 µm for PODs 14 and 21). Mean widths in the rebamipide and control groups on PODs 7, 14, and 21 were 13.8 ± 2.8 ×10³/µm vs. 13.9 ± 2.2 ×10³/µm (P = 0.93), 4.0 ± 1.7 ×10³/µm vs. 5.3 ± 1.9 ×10³/µm (P = 0.33), and 2.3 ± 1.6 ×10³/µm vs. 3.5 ± 2.2 ×10³/µm (P = 0.37), respectively. Although widths tended to be shorter in the rebamipide group on PODs 14 and 21, no statistically significant differences were detected. Linear mixed‑effects analysis revealed no significant group-time interaction. α-SMA, α-smooth muscle actin; POD, postoperative day.
    Nti α Sma Apc, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Proteintech α sma primary antibody
    Histopathologic evaluation of ulcer healing. a Thickness of granulation tissue and representative images of Azan-Mallory staining in the rebamipide and control groups on POD 7 (Scale bar, 1000 µm). The rebamipide group exhibited a greater thickness of granulation tissue compared with the control group (718.0 ± 144.0 µm vs. 589.6 ± 84.9 µm), although this difference did not reach statistical significance (P = 0.12). b The number of microvessels and representative images <t>of</t> <t>α-SMA</t> sections in the rebamipide and control groups on POD 7 (Scale bar, 50 µm). Although the rebamipide group showed a greater number of microvessels (17.0 ± 3.4 vs. 13.8 ± 1.5), the difference was not statistically significant (P = 0.10). c Widths of absent muscularis mucosae and representative images of Azan Mallory staining in the rebamipide and control groups on PODs 7, 14 and 21 (Scale bar, 2500 µm for POD 7; 1000 µm for PODs 14 and 21). Mean widths in the rebamipide and control groups on PODs 7, 14, and 21 were 13.8 ± 2.8 ×10³/µm vs. 13.9 ± 2.2 ×10³/µm (P = 0.93), 4.0 ± 1.7 ×10³/µm vs. 5.3 ± 1.9 ×10³/µm (P = 0.33), and 2.3 ± 1.6 ×10³/µm vs. 3.5 ± 2.2 ×10³/µm (P = 0.37), respectively. Although widths tended to be shorter in the rebamipide group on PODs 14 and 21, no statistically significant differences were detected. Linear mixed‑effects analysis revealed no significant group-time interaction. α-SMA, α-smooth muscle actin; POD, postoperative day.
    α Sma Primary Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/%CE%B1+smooth+muscle+actin+sma+antibody/pm41933369-130-1-9?v=Proteintech
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    Cell Signaling Technology Inc alpha smooth muscle actin α sma antibody
    Histopathologic evaluation of ulcer healing. a Thickness of granulation tissue and representative images of Azan-Mallory staining in the rebamipide and control groups on POD 7 (Scale bar, 1000 µm). The rebamipide group exhibited a greater thickness of granulation tissue compared with the control group (718.0 ± 144.0 µm vs. 589.6 ± 84.9 µm), although this difference did not reach statistical significance (P = 0.12). b The number of microvessels and representative images <t>of</t> <t>α-SMA</t> sections in the rebamipide and control groups on POD 7 (Scale bar, 50 µm). Although the rebamipide group showed a greater number of microvessels (17.0 ± 3.4 vs. 13.8 ± 1.5), the difference was not statistically significant (P = 0.10). c Widths of absent muscularis mucosae and representative images of Azan Mallory staining in the rebamipide and control groups on PODs 7, 14 and 21 (Scale bar, 2500 µm for POD 7; 1000 µm for PODs 14 and 21). Mean widths in the rebamipide and control groups on PODs 7, 14, and 21 were 13.8 ± 2.8 ×10³/µm vs. 13.9 ± 2.2 ×10³/µm (P = 0.93), 4.0 ± 1.7 ×10³/µm vs. 5.3 ± 1.9 ×10³/µm (P = 0.33), and 2.3 ± 1.6 ×10³/µm vs. 3.5 ± 2.2 ×10³/µm (P = 0.37), respectively. Although widths tended to be shorter in the rebamipide group on PODs 14 and 21, no statistically significant differences were detected. Linear mixed‑effects analysis revealed no significant group-time interaction. α-SMA, α-smooth muscle actin; POD, postoperative day.
    Alpha Smooth Muscle Actin α Sma Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/%CE%B1+smooth+muscle+actin+sma+antibody/pm41873577-46-6-12?v=Cell+Signaling+Technology+Inc
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    Image Search Results


    Efficacy of GelMA MAVP MPs in promoting nerve end interface self-resolution. ( A ) Schematic of the peripheral sciatic nerve ligation (p-SNL) model with four experimental groups (i.e., MAVP, VAN, vehicle, and control) ( B ) Immunofluorescence (IF) staining of p-VEGFR2 and YAP (indicating mechanotransduction signaling). ( C ) The positive area percentage of p-VEGFR2 (n = 6). ( D ) Percentage of YAP in nuclear/cytoplasm (n = 6). ( E ) IF staining of proliferation signal (Ki-67) and vessel signal (CD31) for p-SNL animal. ( F ) Quantification of Ki-67/CD31 co-localization area percentage (n = 6). ( G ) IF co-staining of Ki-67 and macrophage marker F4/80. ( H ) Quantification of Ki-67/F4/80 co-localization area percentage (n = 6). ( I ) IF staining of scar marker α-SMA. ( J ) Quantification of α-SMA-positive area percentage (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , D , F , H and J ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Targeting VEGFR2 inhibition within a spatially-confined conduit promotes nerve self-resolution and alleviates mechanical allodynia

    doi: 10.1016/j.bioactmat.2026.03.009

    Figure Lengend Snippet: Efficacy of GelMA MAVP MPs in promoting nerve end interface self-resolution. ( A ) Schematic of the peripheral sciatic nerve ligation (p-SNL) model with four experimental groups (i.e., MAVP, VAN, vehicle, and control) ( B ) Immunofluorescence (IF) staining of p-VEGFR2 and YAP (indicating mechanotransduction signaling). ( C ) The positive area percentage of p-VEGFR2 (n = 6). ( D ) Percentage of YAP in nuclear/cytoplasm (n = 6). ( E ) IF staining of proliferation signal (Ki-67) and vessel signal (CD31) for p-SNL animal. ( F ) Quantification of Ki-67/CD31 co-localization area percentage (n = 6). ( G ) IF co-staining of Ki-67 and macrophage marker F4/80. ( H ) Quantification of Ki-67/F4/80 co-localization area percentage (n = 6). ( I ) IF staining of scar marker α-SMA. ( J ) Quantification of α-SMA-positive area percentage (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( C , D , F , H and J ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: The following primary antibodies were used for the subsequent steps: anti-Yap (mouse, 1:200, Santa sc-376830); anti-p-VEGFR2 (rabbit, 1:100 Invitrogen, PA5-105765); α-SMA (rabbit, 1:200, Proteintech 14395-1-AP); Reca-1 (mouse, 1:200, Santa sc-52665); anti-CD31 (mouse, 1:200, Santa sc-13537); anti-Ki67 (rabbit, 1:150, Cell Signaling 9129S); anti-NF-200 (mouse, 1:200, Sigma, SAB4200747); anti-MBP (rabbit, 1:200, Abcam ab218011); anti-F4/80 (mouse, 1:200, Santa sc-377009); Iba-1 (rabbit, 1:150, Abcam ab178846); anti-CGRP (rabbit, 1:400, Abcam ab283568); anti-TRPA1 (mouse, 1:200, Santa sc-376495); anti-CD86 (rabbit, 1:200, Proteintech 30691-1-AP); CD206 (rabbit, 1:200, Proteintech 18704-1-AP).

    Techniques: Ligation, Control, Immunofluorescence, Staining, Marker

    Expression of pain signal proteins in peripheral nerve locations. ( A ) Immunohistochemical (IHC) imaging of VEGFA and ( B ) quantification of VEGFA mean integrated density (n = 6). ( C ) IHC staining for NGF and ( D ) quantification of NGF mean integrated density (n = 6). ( E ) IF staining for macrophages (F4/80) and ( F ) quantification of macrophage number per 10 4 μm 2 (n = 6). ( G ) IF staining for scar tissue (α-SMA) and ( H ) quantification of α-SMA -positive area percentage (n = 6). ( I ) IF staining for myelin sheath (MBP) and axon (NF200) and ( J ) quantification of myelin sheath to axon area ratio (n = 6). ( K ) IF staining for pain-related mediators CGRP and TRPA1 and ( L ) quantification of CGRP (n = 6), and ( M ) TRPA1 (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( B , D , F , H , J , L and M ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Journal: Bioactive Materials

    Article Title: Targeting VEGFR2 inhibition within a spatially-confined conduit promotes nerve self-resolution and alleviates mechanical allodynia

    doi: 10.1016/j.bioactmat.2026.03.009

    Figure Lengend Snippet: Expression of pain signal proteins in peripheral nerve locations. ( A ) Immunohistochemical (IHC) imaging of VEGFA and ( B ) quantification of VEGFA mean integrated density (n = 6). ( C ) IHC staining for NGF and ( D ) quantification of NGF mean integrated density (n = 6). ( E ) IF staining for macrophages (F4/80) and ( F ) quantification of macrophage number per 10 4 μm 2 (n = 6). ( G ) IF staining for scar tissue (α-SMA) and ( H ) quantification of α-SMA -positive area percentage (n = 6). ( I ) IF staining for myelin sheath (MBP) and axon (NF200) and ( J ) quantification of myelin sheath to axon area ratio (n = 6). ( K ) IF staining for pain-related mediators CGRP and TRPA1 and ( L ) quantification of CGRP (n = 6), and ( M ) TRPA1 (n = 6). Mean values are shown and error bars represent ± s.d., as analyzed by one-way ANOVA followed by the Tukey-Kramer test in ( B , D , F , H , J , L and M ). Biological replicates were used for all experiments. ns, p > 0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

    Article Snippet: The following primary antibodies were used for the subsequent steps: anti-Yap (mouse, 1:200, Santa sc-376830); anti-p-VEGFR2 (rabbit, 1:100 Invitrogen, PA5-105765); α-SMA (rabbit, 1:200, Proteintech 14395-1-AP); Reca-1 (mouse, 1:200, Santa sc-52665); anti-CD31 (mouse, 1:200, Santa sc-13537); anti-Ki67 (rabbit, 1:150, Cell Signaling 9129S); anti-NF-200 (mouse, 1:200, Sigma, SAB4200747); anti-MBP (rabbit, 1:200, Abcam ab218011); anti-F4/80 (mouse, 1:200, Santa sc-377009); Iba-1 (rabbit, 1:150, Abcam ab178846); anti-CGRP (rabbit, 1:400, Abcam ab283568); anti-TRPA1 (mouse, 1:200, Santa sc-376495); anti-CD86 (rabbit, 1:200, Proteintech 30691-1-AP); CD206 (rabbit, 1:200, Proteintech 18704-1-AP).

    Techniques: Expressing, Immunohistochemical staining, Imaging, Immunohistochemistry, Staining

    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin; ns, not significant.

    Journal: Molecular Medicine Reports

    Article Title: Long non-coding RNA NKILA regulates the JAK2/STAT3 pathway to exacerbate TGF-β1-mediated renal fibrosis

    doi: 10.3892/mmr.2026.13839

    Figure Lengend Snippet: Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA overexpression virus (A) Representative western blotting images and (B) quantification of EMT phenotypic indicators. (C) Statistical analysis results of E-cad fluorescence intensity (n=3). (D) RT-qPCR statistical results of EMT phenotype indicators (n=3). ‘Normal’ indicates after starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. Control, following starvation treatment, 10 ng/ml TGF-β1 cytokine diluent was added to induce HK-2 cells to construct the renal interstitial fibrosis model for 24 h. ‘OE-NKILA’ indicates after starvation, overexpressed Lv-NKILA (76304) was used for transfection and cells were collected after 24 h of lentivirus transfection. Compared with OE-NC ## P<0.01. E-cad; epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; EMT, epithelial-mesenchymal transition; NC, negative control; Lv, lentivirus; OE, overexpression; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin; ns, not significant.

    Article Snippet: After blocking with 5% non-fat milk for 2 h at room temperature, membranes were incubated overnight at 4°C with primary antibodies against fibronectin (FN; 1:1,000; cat. no. ab45688; Abcam), collagen I (Col1; 1:1,000; cat. no. ab138492; Abcam), vimentin (Vim; 1:1,000; cat. no. 10366-1-AP; Proteintech Group, Inc.), α-smooth muscle actin (α-SMA; 1:1,000; cat. no. 14395-1-AP; Proteintech Group, Inc.), JAK2 (1:1,000; cat. no. 17670-1-AP; Proteintech Group, Inc.), STAT3 (1:1,000; cat. no. 10253-2-AP; Proteintech Group, Inc.), phosphorylated (p)-JAK2 (1:500; cat. no. ab32101; Abcam), p-STAT3 (1:500; cat. no. ab76315; Abcam) and GAPDH (1:5,000; cat. no. 10494-1-AP; Proteintech Group, Inc.).

    Techniques: Transfection, Over Expression, Virus, Western Blot, Fluorescence, Quantitative RT-PCR, Cell Culture, Control, Construct, Reverse Transcription, Real-time Polymerase Chain Reaction, Negative Control

    Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA knockdown lentivirus (A) Representative western blotting bands and (B) semi-quantification results of EMT phenotypic indicators. (C) E-cad fluorescence intensity and (D) EMT phenotypic index RT-qPCR (n=3). ‘Normal’ indicates starvation treatment. Compared with normal group ## P<0.01. Compared with control + KD-NC group, **P<0.01 and *P<0.05. EMT, epithelial-mesenchymal transition; E-cad, epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; KD, knockdown; Lv, lentivirus; shRNA, short hairpin RNA; NC, negative control; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin.

    Journal: Molecular Medicine Reports

    Article Title: Long non-coding RNA NKILA regulates the JAK2/STAT3 pathway to exacerbate TGF-β1-mediated renal fibrosis

    doi: 10.3892/mmr.2026.13839

    Figure Lengend Snippet: Partial EMT phenotype proteins in HK-2 cells transfected with lncRNA NKILA knockdown lentivirus (A) Representative western blotting bands and (B) semi-quantification results of EMT phenotypic indicators. (C) E-cad fluorescence intensity and (D) EMT phenotypic index RT-qPCR (n=3). ‘Normal’ indicates starvation treatment. Compared with normal group ## P<0.01. Compared with control + KD-NC group, **P<0.01 and *P<0.05. EMT, epithelial-mesenchymal transition; E-cad, epithelial-cadherin; RT-qPCR, reverse transcription quantitative PCR; KD, knockdown; Lv, lentivirus; shRNA, short hairpin RNA; NC, negative control; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin.

    Article Snippet: After blocking with 5% non-fat milk for 2 h at room temperature, membranes were incubated overnight at 4°C with primary antibodies against fibronectin (FN; 1:1,000; cat. no. ab45688; Abcam), collagen I (Col1; 1:1,000; cat. no. ab138492; Abcam), vimentin (Vim; 1:1,000; cat. no. 10366-1-AP; Proteintech Group, Inc.), α-smooth muscle actin (α-SMA; 1:1,000; cat. no. 14395-1-AP; Proteintech Group, Inc.), JAK2 (1:1,000; cat. no. 17670-1-AP; Proteintech Group, Inc.), STAT3 (1:1,000; cat. no. 10253-2-AP; Proteintech Group, Inc.), phosphorylated (p)-JAK2 (1:500; cat. no. ab32101; Abcam), p-STAT3 (1:500; cat. no. ab76315; Abcam) and GAPDH (1:5,000; cat. no. 10494-1-AP; Proteintech Group, Inc.).

    Techniques: Transfection, Knockdown, Western Blot, Fluorescence, Quantitative RT-PCR, Control, Reverse Transcription, Real-time Polymerase Chain Reaction, shRNA, Negative Control

    Detection of EMT-related phenotypic proteins in the AG490 intervention HK-2 cell recovery experiment (A) Representative western blotting bands and (B) semi-quantification of EMT phenotypic protein changes (n=3). (C) Statistical analysis results of E-cad fluorescence intensity (n=3) and (D) EMT phenotypic index through reverse transcription quantitative PCR (n=3). ‘Normal’ indicates starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. ## P<0.01 compared with the normal group, ** P<0.01 and *P<0.05 compared with the control + DMSO group and △△ P<0.01 and △ P<0.05 compared with the OE-NKILA group. EMT, epithelial-mesenchymal transition; E-cad, epithelial cadherin; OE, overexpression; Lv, lentivirus; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin.

    Journal: Molecular Medicine Reports

    Article Title: Long non-coding RNA NKILA regulates the JAK2/STAT3 pathway to exacerbate TGF-β1-mediated renal fibrosis

    doi: 10.3892/mmr.2026.13839

    Figure Lengend Snippet: Detection of EMT-related phenotypic proteins in the AG490 intervention HK-2 cell recovery experiment (A) Representative western blotting bands and (B) semi-quantification of EMT phenotypic protein changes (n=3). (C) Statistical analysis results of E-cad fluorescence intensity (n=3) and (D) EMT phenotypic index through reverse transcription quantitative PCR (n=3). ‘Normal’ indicates starvation treatment, HK-2 cells were replaced with fresh complete medium and continued to be cultured for 24 h. ## P<0.01 compared with the normal group, ** P<0.01 and *P<0.05 compared with the control + DMSO group and △△ P<0.01 and △ P<0.05 compared with the OE-NKILA group. EMT, epithelial-mesenchymal transition; E-cad, epithelial cadherin; OE, overexpression; Lv, lentivirus; FN, fibronectin; Col1, collagen I; α-SMA, α-smooth muscle actin; Vim; vimentin.

    Article Snippet: After blocking with 5% non-fat milk for 2 h at room temperature, membranes were incubated overnight at 4°C with primary antibodies against fibronectin (FN; 1:1,000; cat. no. ab45688; Abcam), collagen I (Col1; 1:1,000; cat. no. ab138492; Abcam), vimentin (Vim; 1:1,000; cat. no. 10366-1-AP; Proteintech Group, Inc.), α-smooth muscle actin (α-SMA; 1:1,000; cat. no. 14395-1-AP; Proteintech Group, Inc.), JAK2 (1:1,000; cat. no. 17670-1-AP; Proteintech Group, Inc.), STAT3 (1:1,000; cat. no. 10253-2-AP; Proteintech Group, Inc.), phosphorylated (p)-JAK2 (1:500; cat. no. ab32101; Abcam), p-STAT3 (1:500; cat. no. ab76315; Abcam) and GAPDH (1:5,000; cat. no. 10494-1-AP; Proteintech Group, Inc.).

    Techniques: Cell Recovery, Western Blot, Fluorescence, Reverse Transcription, Real-time Polymerase Chain Reaction, Cell Culture, Control, Over Expression

    Effects of CoQ10 on fibrosis-related proteins in rat lung tissue induced by SiO 2 dust suspension. ( (A) Effect of CoQ10 on HYP content in rat lungs induced by silica dust; (B) Effect of CoQ10 on the expression of EMT-related proteins in rat lungs induced by silica dust; (C) E-cad protein expression level; (D) Vimentin protein expression level; (E) α-SMA protein expression level; (F) Immunohistochemical detection of α-SMA protein expression (10×); (G) α-SMA protein positive expression level; (H) Effect of CoQ10 on collagen protein expression in rat lung tissue induced by silica dust; (I) Collagen-I protein expression level; (J) Collagen-III protein expression level. Note: * indicates P < 0.05 compared with the Control group; ** indicates P < 0.01 compared with the Control group; # indicates P < 0.05 compared with the Silicosis Model group; ## indicates P < 0.01 compared with the Silicosis Model group. All data are presented as mean ± standard deviation (M ± SD), n = 3).

    Journal: Frontiers in Pharmacology

    Article Title: Coenzyme Q10 alleviates silicotic fibrosis in rats through the TGF-β1/Smad pathway

    doi: 10.3389/fphar.2026.1821205

    Figure Lengend Snippet: Effects of CoQ10 on fibrosis-related proteins in rat lung tissue induced by SiO 2 dust suspension. ( (A) Effect of CoQ10 on HYP content in rat lungs induced by silica dust; (B) Effect of CoQ10 on the expression of EMT-related proteins in rat lungs induced by silica dust; (C) E-cad protein expression level; (D) Vimentin protein expression level; (E) α-SMA protein expression level; (F) Immunohistochemical detection of α-SMA protein expression (10×); (G) α-SMA protein positive expression level; (H) Effect of CoQ10 on collagen protein expression in rat lung tissue induced by silica dust; (I) Collagen-I protein expression level; (J) Collagen-III protein expression level. Note: * indicates P < 0.05 compared with the Control group; ** indicates P < 0.01 compared with the Control group; # indicates P < 0.05 compared with the Silicosis Model group; ## indicates P < 0.01 compared with the Silicosis Model group. All data are presented as mean ± standard deviation (M ± SD), n = 3).

    Article Snippet: Free silica dust (SiO 2 , with ≥80% of particles measuring 0.5–5 μm, Sigma-Aldrich, United States); Coenzyme Q10 (Macklin Biochemical Technology Co., Ltd., Shanghai, China); Kits for Interleukin-1β (IL-1β), Tumor Necrosis Factor-α (TNF-α), Superoxide Dismutase (SOD), and Malondialdehyde (MDA) (Nanjing Jiancheng Bioengineering Institute, China); Hematoxylin and Eosin (H&E) staining solution, Mayer’s Hematoxylin, Eosin Y solution, Masson’s Trichrome Stain Kit, Reactive Oxygen Species (ROS) Staining Kit (Wuhan Biqindu Biotechnology Co., Ltd., China); Tween 20, Rapid Wright-Giemsa Stain, Bicinchoninic Acid (BCA) Protein Assay Kit (Beijing Dingguo Changsheng Biotechnology Co., Ltd., China); Antibodies against α-Smooth Muscle Actin (α-SMA), E-cadherin (E-cad), Vimentin, Collagen Type III (Col-III), Smad2, Smad3 (Abclonal Technology Co., Ltd., Wuhan, China); Antibodies against Collagen Type I (Col-I), Smad7 (Wuhan Sanying Biotechnology Co., Ltd., China); Antibody against Transforming Growth Factor Beta 1 (TGF-β1) (Abcam, China); Horseradish Peroxidase (HRP)-conjugated Goat Anti-Rabbit antibody (Abclonal, China).

    Techniques: Suspension, Expressing, Immunohistochemical staining, Control, Standard Deviation

    Histopathologic evaluation of ulcer healing. a Thickness of granulation tissue and representative images of Azan-Mallory staining in the rebamipide and control groups on POD 7 (Scale bar, 1000 µm). The rebamipide group exhibited a greater thickness of granulation tissue compared with the control group (718.0 ± 144.0 µm vs. 589.6 ± 84.9 µm), although this difference did not reach statistical significance (P = 0.12). b The number of microvessels and representative images of α-SMA sections in the rebamipide and control groups on POD 7 (Scale bar, 50 µm). Although the rebamipide group showed a greater number of microvessels (17.0 ± 3.4 vs. 13.8 ± 1.5), the difference was not statistically significant (P = 0.10). c Widths of absent muscularis mucosae and representative images of Azan Mallory staining in the rebamipide and control groups on PODs 7, 14 and 21 (Scale bar, 2500 µm for POD 7; 1000 µm for PODs 14 and 21). Mean widths in the rebamipide and control groups on PODs 7, 14, and 21 were 13.8 ± 2.8 ×10³/µm vs. 13.9 ± 2.2 ×10³/µm (P = 0.93), 4.0 ± 1.7 ×10³/µm vs. 5.3 ± 1.9 ×10³/µm (P = 0.33), and 2.3 ± 1.6 ×10³/µm vs. 3.5 ± 2.2 ×10³/µm (P = 0.37), respectively. Although widths tended to be shorter in the rebamipide group on PODs 14 and 21, no statistically significant differences were detected. Linear mixed‑effects analysis revealed no significant group-time interaction. α-SMA, α-smooth muscle actin; POD, postoperative day.

    Journal: Endoscopy International Open

    Article Title: Use of rebamipide solution as a submucosal injection material to prevent esophageal stricture after endoscopic submucosal dissection: Animal study

    doi: 10.1055/a-2820-3721

    Figure Lengend Snippet: Histopathologic evaluation of ulcer healing. a Thickness of granulation tissue and representative images of Azan-Mallory staining in the rebamipide and control groups on POD 7 (Scale bar, 1000 µm). The rebamipide group exhibited a greater thickness of granulation tissue compared with the control group (718.0 ± 144.0 µm vs. 589.6 ± 84.9 µm), although this difference did not reach statistical significance (P = 0.12). b The number of microvessels and representative images of α-SMA sections in the rebamipide and control groups on POD 7 (Scale bar, 50 µm). Although the rebamipide group showed a greater number of microvessels (17.0 ± 3.4 vs. 13.8 ± 1.5), the difference was not statistically significant (P = 0.10). c Widths of absent muscularis mucosae and representative images of Azan Mallory staining in the rebamipide and control groups on PODs 7, 14 and 21 (Scale bar, 2500 µm for POD 7; 1000 µm for PODs 14 and 21). Mean widths in the rebamipide and control groups on PODs 7, 14, and 21 were 13.8 ± 2.8 ×10³/µm vs. 13.9 ± 2.2 ×10³/µm (P = 0.93), 4.0 ± 1.7 ×10³/µm vs. 5.3 ± 1.9 ×10³/µm (P = 0.33), and 2.3 ± 1.6 ×10³/µm vs. 3.5 ± 2.2 ×10³/µm (P = 0.37), respectively. Although widths tended to be shorter in the rebamipide group on PODs 14 and 21, no statistically significant differences were detected. Linear mixed‑effects analysis revealed no significant group-time interaction. α-SMA, α-smooth muscle actin; POD, postoperative day.

    Article Snippet: Serial sections were cut for immunostaining using the mouse monoclonal anti-α-smooth muscle actin (α-SMA) antibody (1:400 dilution, 1A4/asm-1; Novus Biologicals, Littleton, Colorado, United States).

    Techniques: Staining, Control

    Histopathologic evaluation of fibrosis formation. a Proportion of α-SMA-positive cells and representative images of α-SMA sections in the rebamipide and control groups on PODs 7, 14, and 21 (Scale bar, 50 µm). Proportions of α‑SMA–positive cells in the rebamipide and control groups on PODs 7, 14, and 21 were 29.0 ± 9.1% vs. 35.1 ± 9.0% (P = 0.22), 24.3 ± 7.9% vs. 27.4 ± 7.5% (P = 0.52), and 19.2 ± 2.2% vs. 25.8 ± 7.4% (P = 0.18), respectively ( a ). Although none of these differences were statistically significant, the rebamipide group consistently showed lower proportions of α‑SMA–positive cells across all time points. Linear mixed‑effects analysis revealed no significant group–time interaction. b Thickness of fibrosis and representative images of Azan-Mallory staining in the rebamipide and control groups on PODs 7, 14, and 21 (Scale bar, 500 µm). Thickness of fibrosis in the rebamipide and control groups on PODs 7, 14, and 21 was 558.6 ± 169.7 µm vs. 450.8 ± 131.1 µm (P = 0.58), 807.0 ± 238.9 µm vs. 972.8 ± 395.1 µm (P = 0.40), and 782.8 ± 281.5 µm vs. 1087.0 ± 476.0 µm (P = 0.13), respectively. Fibrosis progressed on POD 7 but was attenuated on PODs 14 and 21 in the rebamipide group compared with the control group. Linear mixed‑effects analysis demonstrated a significant group–time interaction, with the between‑group difference becoming evident at POD 21 (P = 0.049). α-SMA, α-smooth muscle actin; POD, postoperative day

    Journal: Endoscopy International Open

    Article Title: Use of rebamipide solution as a submucosal injection material to prevent esophageal stricture after endoscopic submucosal dissection: Animal study

    doi: 10.1055/a-2820-3721

    Figure Lengend Snippet: Histopathologic evaluation of fibrosis formation. a Proportion of α-SMA-positive cells and representative images of α-SMA sections in the rebamipide and control groups on PODs 7, 14, and 21 (Scale bar, 50 µm). Proportions of α‑SMA–positive cells in the rebamipide and control groups on PODs 7, 14, and 21 were 29.0 ± 9.1% vs. 35.1 ± 9.0% (P = 0.22), 24.3 ± 7.9% vs. 27.4 ± 7.5% (P = 0.52), and 19.2 ± 2.2% vs. 25.8 ± 7.4% (P = 0.18), respectively ( a ). Although none of these differences were statistically significant, the rebamipide group consistently showed lower proportions of α‑SMA–positive cells across all time points. Linear mixed‑effects analysis revealed no significant group–time interaction. b Thickness of fibrosis and representative images of Azan-Mallory staining in the rebamipide and control groups on PODs 7, 14, and 21 (Scale bar, 500 µm). Thickness of fibrosis in the rebamipide and control groups on PODs 7, 14, and 21 was 558.6 ± 169.7 µm vs. 450.8 ± 131.1 µm (P = 0.58), 807.0 ± 238.9 µm vs. 972.8 ± 395.1 µm (P = 0.40), and 782.8 ± 281.5 µm vs. 1087.0 ± 476.0 µm (P = 0.13), respectively. Fibrosis progressed on POD 7 but was attenuated on PODs 14 and 21 in the rebamipide group compared with the control group. Linear mixed‑effects analysis demonstrated a significant group–time interaction, with the between‑group difference becoming evident at POD 21 (P = 0.049). α-SMA, α-smooth muscle actin; POD, postoperative day

    Article Snippet: Serial sections were cut for immunostaining using the mouse monoclonal anti-α-smooth muscle actin (α-SMA) antibody (1:400 dilution, 1A4/asm-1; Novus Biologicals, Littleton, Colorado, United States).

    Techniques: Control, Staining