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96
ABclonal Biotechnology α sma
In vivo evaluation of re-endothelialization and inhibition of intimal hyperplasia following stent implantation. (A–E) SEM images of the luminal surface treated with EV-loaded (A, B) or DPBS-loaded (D, E) nanofibrous membranes. The EV-treated group exhibited a continuous, smooth, and intact endothelial layer (A, B), whereas the DPBS group displayed incomplete coverage with substantial endothelial disruption (D, E). (C, F) H&E-stained cross-sections revealed the extent of neointimal formation above the stent struts (black arrows). The EV group (C) demonstrated significantly reduced intimal thickening compared with the pronounced hyperplasia observed in the DPBS group (F). (G–H) Statistical analysis confirmed that EV treatment significantly increased endothelial coverage (G) and suppressed intimal hyperplasia thickness (H). (I–K) EV treatment significantly upregulated the expression of the angiogenic factor VEGF (I), the endothelial marker CD31 (J), and the proliferation marker PCNA (K), confirming accelerated vascular repair. (L–N) EV treatment prevented phenotypic switching and matrix accumulation, as evidenced by reduced levels of the contractile/hyperplasia <t>marker</t> <t>α-SMA</t> (L). Furthermore, the EV group showed decreased expression of matrix metalloproteinases MMP-2 and MMP-9 (M) and beneficial modulation of collagen composition, with increased Collagen I and the Collagen I/III ratio (N). (O–P) The EV group exhibited significantly downregulated levels of the profibrotic factor TGF-β1 (O) and the inflammatory cytokine IL-6 (P). N = 5 (G and H), and n = 3 (I-P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.000.
α Sma, supplied by ABclonal Biotechnology, 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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ABclonal Biotechnology α sma antibodies
Effect of fisetin on fibrosis <t>biomarkers</t> <t>(TGF‐β1</t> and <t>α‐SMA).</t> (A) Immunostaining of TGF‐β1 and α‐SMA in the uterine tissues of different animal groups. In the control and FIS groups, TGF‐β1 expression was minimal in stromal cells and mononuclear immune cells. In the induction group, TGF‐β1 expression was prominent in stromal cells between muscle (green arrow) and within immune cells in the endometrial tissue (blue arrow). The UL + FIS group exhibited a significant decrease in TGF‐β1 expression in stromal and immune cells (blue arrow). Regarding α‐SMA, its expression in smooth muscle cells highlights myometrial thickness of approximately 4 mm and 4.5 mm in the control and FIS groups, respectively. In the induction group, α‐SMA expression indicates a notable increase in myometrial thickness, reaching 12 mm. In the UL + FIS group, α‐SMA expression shows a substantial reduction in myometrial thickness compared to the induction group, decreasing to about 6 mm (×40). (B) Relative mRNA expression of TGF‐β1. n = 10in each group. β‐actin was used to normalize expression data. Data are presented as means ± S.D. ** p ≤ 0.01, *** p ≤ 0.001 versus control group; $$ p ≤ 0.01, $$$ p ≤ 0.001 versus FIS‐treated group; ## p ≤ 0.01 versus UL group. FIS, fisetin; TGF‐β1, transforming growth factor β1; α‐SMA, α‐ α‐smooth muscle actin; UL, uterine leiomyoma; UL + FIS, uterine leiomyoma + fisetin.
α Sma Antibodies, supplied by ABclonal Biotechnology, 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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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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Servicebio Inc anti 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.
Anti α Sma, supplied by Servicebio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ABclonal Biotechnology α sma acta2
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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ABclonal Biotechnology anti 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.
Anti α Sma, supplied by ABclonal Biotechnology, 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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Image Search Results


In vivo evaluation of re-endothelialization and inhibition of intimal hyperplasia following stent implantation. (A–E) SEM images of the luminal surface treated with EV-loaded (A, B) or DPBS-loaded (D, E) nanofibrous membranes. The EV-treated group exhibited a continuous, smooth, and intact endothelial layer (A, B), whereas the DPBS group displayed incomplete coverage with substantial endothelial disruption (D, E). (C, F) H&E-stained cross-sections revealed the extent of neointimal formation above the stent struts (black arrows). The EV group (C) demonstrated significantly reduced intimal thickening compared with the pronounced hyperplasia observed in the DPBS group (F). (G–H) Statistical analysis confirmed that EV treatment significantly increased endothelial coverage (G) and suppressed intimal hyperplasia thickness (H). (I–K) EV treatment significantly upregulated the expression of the angiogenic factor VEGF (I), the endothelial marker CD31 (J), and the proliferation marker PCNA (K), confirming accelerated vascular repair. (L–N) EV treatment prevented phenotypic switching and matrix accumulation, as evidenced by reduced levels of the contractile/hyperplasia marker α-SMA (L). Furthermore, the EV group showed decreased expression of matrix metalloproteinases MMP-2 and MMP-9 (M) and beneficial modulation of collagen composition, with increased Collagen I and the Collagen I/III ratio (N). (O–P) The EV group exhibited significantly downregulated levels of the profibrotic factor TGF-β1 (O) and the inflammatory cytokine IL-6 (P). N = 5 (G and H), and n = 3 (I-P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.000.

Journal: Materials Today Bio

Article Title: Human iPSC-EV-loaded nanofiber stent coatings accelerate vascular repair by enhancing EGFR/HIF-1α signaling and suppressing ROCK1-mediated remodeling

doi: 10.1016/j.mtbio.2026.103564

Figure Lengend Snippet: In vivo evaluation of re-endothelialization and inhibition of intimal hyperplasia following stent implantation. (A–E) SEM images of the luminal surface treated with EV-loaded (A, B) or DPBS-loaded (D, E) nanofibrous membranes. The EV-treated group exhibited a continuous, smooth, and intact endothelial layer (A, B), whereas the DPBS group displayed incomplete coverage with substantial endothelial disruption (D, E). (C, F) H&E-stained cross-sections revealed the extent of neointimal formation above the stent struts (black arrows). The EV group (C) demonstrated significantly reduced intimal thickening compared with the pronounced hyperplasia observed in the DPBS group (F). (G–H) Statistical analysis confirmed that EV treatment significantly increased endothelial coverage (G) and suppressed intimal hyperplasia thickness (H). (I–K) EV treatment significantly upregulated the expression of the angiogenic factor VEGF (I), the endothelial marker CD31 (J), and the proliferation marker PCNA (K), confirming accelerated vascular repair. (L–N) EV treatment prevented phenotypic switching and matrix accumulation, as evidenced by reduced levels of the contractile/hyperplasia marker α-SMA (L). Furthermore, the EV group showed decreased expression of matrix metalloproteinases MMP-2 and MMP-9 (M) and beneficial modulation of collagen composition, with increased Collagen I and the Collagen I/III ratio (N). (O–P) The EV group exhibited significantly downregulated levels of the profibrotic factor TGF-β1 (O) and the inflammatory cytokine IL-6 (P). N = 5 (G and H), and n = 3 (I-P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.000.

Article Snippet: Smooth muscle and fibrosis markers: α-SMA (1:1000, A17910, ABclonal), SM22α (1:1000, ab14106, Abcam), Calponin-1 (1:1000, ab46794, Abcam), Osteopontin (1:1000, ab8448, Abcam), Collagen I (1:1000, A5786, ABclonal), and Collagen III (1:1000, A3795, ABclonal).

Techniques: In Vivo, Inhibition, Disruption, Staining, Expressing, Marker

Effect of fisetin on fibrosis biomarkers (TGF‐β1 and α‐SMA). (A) Immunostaining of TGF‐β1 and α‐SMA in the uterine tissues of different animal groups. In the control and FIS groups, TGF‐β1 expression was minimal in stromal cells and mononuclear immune cells. In the induction group, TGF‐β1 expression was prominent in stromal cells between muscle (green arrow) and within immune cells in the endometrial tissue (blue arrow). The UL + FIS group exhibited a significant decrease in TGF‐β1 expression in stromal and immune cells (blue arrow). Regarding α‐SMA, its expression in smooth muscle cells highlights myometrial thickness of approximately 4 mm and 4.5 mm in the control and FIS groups, respectively. In the induction group, α‐SMA expression indicates a notable increase in myometrial thickness, reaching 12 mm. In the UL + FIS group, α‐SMA expression shows a substantial reduction in myometrial thickness compared to the induction group, decreasing to about 6 mm (×40). (B) Relative mRNA expression of TGF‐β1. n = 10in each group. β‐actin was used to normalize expression data. Data are presented as means ± S.D. ** p ≤ 0.01, *** p ≤ 0.001 versus control group; $$ p ≤ 0.01, $$$ p ≤ 0.001 versus FIS‐treated group; ## p ≤ 0.01 versus UL group. FIS, fisetin; TGF‐β1, transforming growth factor β1; α‐SMA, α‐ α‐smooth muscle actin; UL, uterine leiomyoma; UL + FIS, uterine leiomyoma + fisetin.

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Fisetin Attenuates Uterine Leiomyoma in Rats: Potential Crosstalk Between HMGB1, SphK1/S1P, and TGF‐β Signaling

doi: 10.1002/jbt.71105

Figure Lengend Snippet: Effect of fisetin on fibrosis biomarkers (TGF‐β1 and α‐SMA). (A) Immunostaining of TGF‐β1 and α‐SMA in the uterine tissues of different animal groups. In the control and FIS groups, TGF‐β1 expression was minimal in stromal cells and mononuclear immune cells. In the induction group, TGF‐β1 expression was prominent in stromal cells between muscle (green arrow) and within immune cells in the endometrial tissue (blue arrow). The UL + FIS group exhibited a significant decrease in TGF‐β1 expression in stromal and immune cells (blue arrow). Regarding α‐SMA, its expression in smooth muscle cells highlights myometrial thickness of approximately 4 mm and 4.5 mm in the control and FIS groups, respectively. In the induction group, α‐SMA expression indicates a notable increase in myometrial thickness, reaching 12 mm. In the UL + FIS group, α‐SMA expression shows a substantial reduction in myometrial thickness compared to the induction group, decreasing to about 6 mm (×40). (B) Relative mRNA expression of TGF‐β1. n = 10in each group. β‐actin was used to normalize expression data. Data are presented as means ± S.D. ** p ≤ 0.01, *** p ≤ 0.001 versus control group; $$ p ≤ 0.01, $$$ p ≤ 0.001 versus FIS‐treated group; ## p ≤ 0.01 versus UL group. FIS, fisetin; TGF‐β1, transforming growth factor β1; α‐SMA, α‐ α‐smooth muscle actin; UL, uterine leiomyoma; UL + FIS, uterine leiomyoma + fisetin.

Article Snippet: For immunohistochemistry analysis, formalin‐fixed, paraffin‐embedded tissue slices were stained for TGF‐β1 and α‐SMA antibodies supplied by Abclonal Inc., China (Cat. No: A16640 and A17910, for TGF‐β1 and α‐SMA, respectively) according to the manufacturer's instructions.

Techniques: Immunostaining, Control, Expressing

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