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Nicotine-stimulated visceral adipose-derived EVs promote atherosclerotic plaque progression and preferentially target plaque-resident macrophages (A) Schematic illustration of the experimental design evaluating the effect of visceral adipose–derived EVs on atherosclerosis. ApoE −/− recipient mice were fed an HFD for 8 weeks, followed by 4 weeks of tail vein injection with EVs isolated from the VAT of HFD-fed or HFD+nicotine (HFD+Ni)-treated donor mice. (B) Representative images of aortic sinuses: gross morphology, H&E-stained sections, and oil red O-stained sections (scale bars, 1 mm for gross images; 200 μm for stained sections). (C) Quantification of atherosclerotic plaque parameters in aortic sinuses based on H&E staining ( n = 8) and lipid accumulation based on oil red O staining ( n = 4). (D) Immunohistochemical staining of aortic sinuses for pro-inflammatory cytokines (IL-6, IL-1β, <t>and</t> <t>TNF-α)</t> and the antioxidant enzyme SOD2 (scale bars, 100 μm). (E) Quantification of expression levels of pro-inflammatory cytokines and antioxidant markers in aortic sinuses ( n = 6). (F and G) Confocal fluorescence images showing co-localization of PKH67-labeled EVs (green) with CD68 + macrophages (red, F) <t>and</t> <t>α-SMA</t> + vascular smooth muscle cells (red, G) in atherosclerotic plaques; DAPI (blue) stains cell nuclei (scale bars, 50 μm in F and 100 μm in G). (H) Quantification of PKH67-labeled EVs co-localized with CD68 + macrophages, demonstrating significantly greater uptake of HFD+Ni EVs by plaque-resident macrophages compared with HFD EVs ( n = 6). Values are shown as mean ± SEM. Two-group comparisons were performed using unpaired two-tailed Student’s t tests. Sample sizes (n) indicate biological replicates per group. ∗p < 0.05 , ∗∗p < 0.01 , ∗∗∗p < 0.001 , ∗∗∗∗p < 0.0001.

α Sma, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1786 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 98 stars, based on 1786 article reviews

α sma - by Bioz Stars, 2026-10

98/100 stars

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1) Product Images from "Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis"

Article Title: Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis

Journal: iScience

doi: 10.1016/j.isci.2026.115151

Figure Legend Snippet: Nicotine-stimulated visceral adipose-derived EVs promote atherosclerotic plaque progression and preferentially target plaque-resident macrophages (A) Schematic illustration of the experimental design evaluating the effect of visceral adipose–derived EVs on atherosclerosis. ApoE −/− recipient mice were fed an HFD for 8 weeks, followed by 4 weeks of tail vein injection with EVs isolated from the VAT of HFD-fed or HFD+nicotine (HFD+Ni)-treated donor mice. (B) Representative images of aortic sinuses: gross morphology, H&E-stained sections, and oil red O-stained sections (scale bars, 1 mm for gross images; 200 μm for stained sections). (C) Quantification of atherosclerotic plaque parameters in aortic sinuses based on H&E staining ( n = 8) and lipid accumulation based on oil red O staining ( n = 4). (D) Immunohistochemical staining of aortic sinuses for pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) and the antioxidant enzyme SOD2 (scale bars, 100 μm). (E) Quantification of expression levels of pro-inflammatory cytokines and antioxidant markers in aortic sinuses ( n = 6). (F and G) Confocal fluorescence images showing co-localization of PKH67-labeled EVs (green) with CD68 + macrophages (red, F) and α-SMA + vascular smooth muscle cells (red, G) in atherosclerotic plaques; DAPI (blue) stains cell nuclei (scale bars, 50 μm in F and 100 μm in G). (H) Quantification of PKH67-labeled EVs co-localized with CD68 + macrophages, demonstrating significantly greater uptake of HFD+Ni EVs by plaque-resident macrophages compared with HFD EVs ( n = 6). Values are shown as mean ± SEM. Two-group comparisons were performed using unpaired two-tailed Student’s t tests. Sample sizes (n) indicate biological replicates per group. ∗p < 0.05 , ∗∗p < 0.01 , ∗∗∗p < 0.001 , ∗∗∗∗p < 0.0001.

Techniques Used: Derivative Assay, Injection, Isolation, Staining, Immunohistochemical staining, Expressing, Fluorescence, Labeling, Two Tailed Test

Incubation:

Article Title: 4D-printed hydrogel with precise regulation of viability and environment of stem cells for diabetic skin wound healing
Article Snippet: The cells were then blocked with blocking buffer (5 % BSA+0.3 % Triton X-100) at room temperature for 1 h. Then the blocking buffer was discarded and incubated with Ki67 (Cell Signaling Technology, 1:150, Alexa Fluor 488 labeled, USA) antibody overnight at 4 °C. .. The tissues were incubated with α-smooth muscle actin (α-SMA) (Cell Signaling Technology, 1:200, USA) antibody overnight at 4 °C and then with Cy3-labeled goat anti-rabbit IgG secondary antibody (Boster Biological Technology Co., Ltd., 1:100, Wuhan, China) for 2 h at room temperature. .. Finally, the tissues were sealed with an anti-fluorescence attenuation tablet containing DAPI (Dalian Meilun Biotechnology Co., Ltd., China).

Article Title: Mechanisms of IL‐17A Neutralisation in Alleviating Renal Fibrosis and Inflammation in Spontaneously Hypertensive Rats
Article Snippet: .. Sections were then incubated overnight at 4°C with primary antibodies against: E‐cadherin (Boster, China), Collagen III (Boster, China), inducible nitric oxide synthase (iNOS) (Boster, China), CD86 (Boster, China), arginase‐1 (Arg‐1) (Boster, China), CD163 (Boster, China), α‐smooth muscle actin (α‐SMA) (Cell Signalling Technology, USA). ..

Article Title: Self-homing TGF-β1 traps: Engineered vasorin vesicles as smart biomaterials for targeted anti-fibrotic therapy after myocardial infarction
Article Snippet: .. Membranes were then incubated overnight at 4 °C with the following primary antibodies: anti-Flag (1:5,000; ABclonal, Hangzhou, China), β3-tubulin (1:10,000; Cell Signaling Technology, Danvers, MA, USA), integrin β3/CD61 (1:1,000; Cell Signaling Technology), matrix metalloproteinase-2 (MMP-2) (1:1,000; Cell Signaling Technology), fibronectin (1:1,000; ABclonal), collagen I (COL1) (1:1,000; ABclonal), α-smooth muscle actin (α-SMA) (1:1,000; Cell Signaling Technology), drosophila mothers against decapentaplegic 2 (SMAD2) (1:1,000; Cell Signaling Technology), phosphorylated SMAD2 (1:1,000; Cell Signaling Technology), and vasorin (1:1,000; Thermo Fisher Scientific Inc.). .. After three 5-min TBST washes, membranes were incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies (goat anti-mouse or anti-rabbit, 1:5,000; Thermo Fisher Scientific Inc.) for 1 h at RT.

other:

Article Title: Artesunate attenuates pulmonary fibrosis by suppressing fibroblast senescence through inhibition of the STAT3/p53 signaling pathway.
Article Snippet: Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and lethal lung disease with elusive pathogenesis.. Accumulating evidence implicates cellular senescence as a key mechanism in IPF.. Current therapies (pirfenidone/nintedanib) reduce acute exacerbation risk and delay lung function decline in mild-tomoderate IPF, but adverse effects often limit their use.

Article Title: Quercus acuta Acorn Bran Extract Enhances Wound Healing by Promoting Human Dermal Fibroblast Migration and Antioxidant Activity.
Article Snippet: We also included antibodies against COL1A1 (#72026), α-smooth muscle actin (α-SMA) (#19245), and vimentin (#5741) from Cell Signaling Technology (Danvers, MA, USA), as well as the antibody for endothelin-1 (ET-1, PA3-067) from Invitrogen.

Article Title: Quercus acuta Acorn Bran Extract Enhances Wound Healing by Promoting Human Dermal Fibroblast Migration and Antioxidant Activity
Article Snippet: We also included antibodies against COL1A1 (#72026), α-smooth muscle actin (α-SMA) (#19245), and vimentin (#5741) from Cell Signaling Technology (Danvers, MA, USA), as well as the antibody for endothelin-1 (ET-1, PA3-067) from Invitrogen.

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.

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.

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.

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

Journal: iScience

Article Title: Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis

doi: 10.1016/j.isci.2026.115151

Figure Lengend Snippet: Nicotine-stimulated visceral adipose-derived EVs promote atherosclerotic plaque progression and preferentially target plaque-resident macrophages (A) Schematic illustration of the experimental design evaluating the effect of visceral adipose–derived EVs on atherosclerosis. ApoE −/− recipient mice were fed an HFD for 8 weeks, followed by 4 weeks of tail vein injection with EVs isolated from the VAT of HFD-fed or HFD+nicotine (HFD+Ni)-treated donor mice. (B) Representative images of aortic sinuses: gross morphology, H&E-stained sections, and oil red O-stained sections (scale bars, 1 mm for gross images; 200 μm for stained sections). (C) Quantification of atherosclerotic plaque parameters in aortic sinuses based on H&E staining ( n = 8) and lipid accumulation based on oil red O staining ( n = 4). (D) Immunohistochemical staining of aortic sinuses for pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) and the antioxidant enzyme SOD2 (scale bars, 100 μm). (E) Quantification of expression levels of pro-inflammatory cytokines and antioxidant markers in aortic sinuses ( n = 6). (F and G) Confocal fluorescence images showing co-localization of PKH67-labeled EVs (green) with CD68 + macrophages (red, F) and α-SMA + vascular smooth muscle cells (red, G) in atherosclerotic plaques; DAPI (blue) stains cell nuclei (scale bars, 50 μm in F and 100 μm in G). (H) Quantification of PKH67-labeled EVs co-localized with CD68 + macrophages, demonstrating significantly greater uptake of HFD+Ni EVs by plaque-resident macrophages compared with HFD EVs ( n = 6). Values are shown as mean ± SEM. Two-group comparisons were performed using unpaired two-tailed Student’s t tests. Sample sizes (n) indicate biological replicates per group. ∗p < 0.05 , ∗∗p < 0.01 , ∗∗∗p < 0.001 , ∗∗∗∗p < 0.0001.

Article Snippet: α-SMA , Cell Signaling Technology , Cat# 19245; RRID: AB_2734735.

Techniques: Derivative Assay, Injection, Isolation, Staining, Immunohistochemical staining, Expressing, Fluorescence, Labeling, Two Tailed Test

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

Techniques: Control, Staining

TAK-981 improves impaired SA remodeling, uteroplacental blood flow and reduces placental SUMOylation. ( A ) Placental SA remodeling. Representative images of pan-CK and α-Sma IF staining in SA (400×). ( B ) Placental morphology. Representative H&E images of labyrinth zone (400×). ( C ) Doppler ultrasonography. ( Left panel ): The representative images of SA, canal and fetal UA visualized by ultrasound biomicroscopy. ( Right panel ): Cumulative data of the PSV of SA, Canal and UA. Error bar, SEM, n = 5 in each group. ( D ) Protein levels of conjugated SUMO1 and SUMO2/3 in placental decidua and placental labyrinth. Error bar, SEM, n = 5 in each group. * p < 0.05, ** p < 0.01.

Journal: Antioxidants

Article Title: SUMOylation Inhibitor TAK-981 Alleviates Hallmark Features of Preeclampsia Related to High Glucocorticoid Exposure by Inhibiting Placental Oxidative Stress in Rats

doi: 10.3390/antiox15040478

Figure Lengend Snippet: TAK-981 improves impaired SA remodeling, uteroplacental blood flow and reduces placental SUMOylation. ( A ) Placental SA remodeling. Representative images of pan-CK and α-Sma IF staining in SA (400×). ( B ) Placental morphology. Representative H&E images of labyrinth zone (400×). ( C ) Doppler ultrasonography. ( Left panel ): The representative images of SA, canal and fetal UA visualized by ultrasound biomicroscopy. ( Right panel ): Cumulative data of the PSV of SA, Canal and UA. Error bar, SEM, n = 5 in each group. ( D ) Protein levels of conjugated SUMO1 and SUMO2/3 in placental decidua and placental labyrinth. Error bar, SEM, n = 5 in each group. * p < 0.05, ** p < 0.01.

Article Snippet: Briefly, after blocking with 5% bovine serum albumin (Servicebio, Wuhan, China), sections were incubated overnight at 4 °C with primary antibodies against pan-cytokeratin (pan-CK) (1:500, Dako, Glostrup, Denmark) or α-smooth muscle actin (α-SMA) (1:400, Servicebio).

Techniques: Staining

Review

α sma (Cell Signaling Technology Inc)

Structured Review

Images

1) Product Images from "Adipose extracellular vesicles carrying miR-210-3p drive macrophage inflammation and nicotine-induced atherosclerosis"

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