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rabbit anti mouse polyclonal antibodies against tlr2  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology rabbit anti mouse polyclonal antibodies against tlr2
    (A–F) Expression of <t>TLR2</t> in lung tissue from the mice in each group was assessed using immunohistochemistry (deep brown cellular area indicates positive staining; magnification, x200). (G) Quantification of TLR2-positive staining in five fields of view per section from each mouse was assessed by JD-801 computer-aided image analyzer under high-power magnification (x200). Values are expressed as the mean ± standard deviation of five mice in each group. * P<0.05, as compared with the NC group. # P<0.05, as compared with the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit IgG-treated AM; TLR, of toll-like receptor.
    Rabbit Anti Mouse Polyclonal Antibodies Against Tlr2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 4689 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/rabbit anti mouse polyclonal antibodies against tlr2/product/Santa Cruz Biotechnology
    Average 96 stars, based on 4689 article reviews
    rabbit anti mouse polyclonal antibodies against tlr2 - by Bioz Stars, 2026-02
    96/100 stars

    Images

    1) Product Images from "Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin"

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2015.3443

    (A–F) Expression of TLR2 in lung tissue from the mice in each group was assessed using immunohistochemistry (deep brown cellular area indicates positive staining; magnification, x200). (G) Quantification of TLR2-positive staining in five fields of view per section from each mouse was assessed by JD-801 computer-aided image analyzer under high-power magnification (x200). Values are expressed as the mean ± standard deviation of five mice in each group. * P<0.05, as compared with the NC group. # P<0.05, as compared with the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit IgG-treated AM; TLR, of toll-like receptor.
    Figure Legend Snippet: (A–F) Expression of TLR2 in lung tissue from the mice in each group was assessed using immunohistochemistry (deep brown cellular area indicates positive staining; magnification, x200). (G) Quantification of TLR2-positive staining in five fields of view per section from each mouse was assessed by JD-801 computer-aided image analyzer under high-power magnification (x200). Values are expressed as the mean ± standard deviation of five mice in each group. * P<0.05, as compared with the NC group. # P<0.05, as compared with the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit IgG-treated AM; TLR, of toll-like receptor.

    Techniques Used: Expressing, Immunohistochemistry, Staining, Standard Deviation, Control

    Expressions of TLR2 and MyD88 assessed using western blot analysis in lung tissue obtained from the mice in each group. The western blot shown is a representative of five independent experiments, and β-actin protein served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) × 100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as mean ± standard deviation of five mice in each group. * P<0.05, as compared with the arbitrary units of the same protein in the NC group. # P<0.05, as compared with the arbitrary units of the same protein in the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit immunoglobulin G-treated AM; MyD88, mycloid differentiation factor 88; TLR, toll-like receptor.
    Figure Legend Snippet: Expressions of TLR2 and MyD88 assessed using western blot analysis in lung tissue obtained from the mice in each group. The western blot shown is a representative of five independent experiments, and β-actin protein served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) × 100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as mean ± standard deviation of five mice in each group. * P<0.05, as compared with the arbitrary units of the same protein in the NC group. # P<0.05, as compared with the arbitrary units of the same protein in the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit immunoglobulin G-treated AM; MyD88, mycloid differentiation factor 88; TLR, toll-like receptor.

    Techniques Used: Western Blot, Control, Standard Deviation

    Supernatant levels of IL-4, IL-6 and IL-8 released from leukocytes exposed to IL-1β were assessed using ELISA. The cultured leukocytes were obtained from a mouse from the normal control group and stimulated with IL-1β (10 ng/ml) for 24 h with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h and TPCA-1 (10 μ M) for 1 h. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the levels of same cytokine released from the cells without treatment. # P<0.05, as compared to the levels of same cytokine released from the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin G; TLR, toll-like receptor; TPCA-1,10, thiophene-3-carboxamide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.
    Figure Legend Snippet: Supernatant levels of IL-4, IL-6 and IL-8 released from leukocytes exposed to IL-1β were assessed using ELISA. The cultured leukocytes were obtained from a mouse from the normal control group and stimulated with IL-1β (10 ng/ml) for 24 h with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h and TPCA-1 (10 μ M) for 1 h. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the levels of same cytokine released from the cells without treatment. # P<0.05, as compared to the levels of same cytokine released from the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin G; TLR, toll-like receptor; TPCA-1,10, thiophene-3-carboxamide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Techniques Used: Enzyme-linked Immunosorbent Assay, Cell Culture, Control, Standard Deviation

    Expression of TLR2 and MyD88 assessed using western blot analysis of leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 30 min with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h and MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h. The western blot is representative of five independent experiments, and the lower panel shows β-actin protein, which served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) ×100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. # P<0.05, as compared to the arbitrary units of the same protein in the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin; TLR, toll-like receptor; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.
    Figure Legend Snippet: Expression of TLR2 and MyD88 assessed using western blot analysis of leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 30 min with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h and MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h. The western blot is representative of five independent experiments, and the lower panel shows β-actin protein, which served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) ×100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. # P<0.05, as compared to the arbitrary units of the same protein in the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin; TLR, toll-like receptor; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Techniques Used: Expressing, Western Blot, Cell Culture, Control, Standard Deviation

    Activation of NF-κB assessed using western blot analysis in leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 1 h with or without pre-treatment of BML-111 (1 mM) for 30 min, BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, ST2825 (20 μ M) for 1 h or TPCA-1 (10 μ M) for 1 h. The western blot is representative of five independent experiments. GAPDH served as a loading control of cytosolic proteins. Histone 3 protein served as a loading control of nuclear proteins. Semiquantitative analysis was performed using UVP-gel densitometry. Arbitrary unit = (A IκBα /A GAPDH ) ×100%, or (A cytosolic p65 /A GAPDH ) ×100%, or (A nuclear p65 /A histone 3 ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. IL, interleukin; IgG, immunoglobulin G; TPCA-1,10, thiophene-3-carbox-amide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe; NF-κB, nuclear factor-κB; IκBα, inhibitor of kappa B alpha.
    Figure Legend Snippet: Activation of NF-κB assessed using western blot analysis in leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 1 h with or without pre-treatment of BML-111 (1 mM) for 30 min, BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, ST2825 (20 μ M) for 1 h or TPCA-1 (10 μ M) for 1 h. The western blot is representative of five independent experiments. GAPDH served as a loading control of cytosolic proteins. Histone 3 protein served as a loading control of nuclear proteins. Semiquantitative analysis was performed using UVP-gel densitometry. Arbitrary unit = (A IκBα /A GAPDH ) ×100%, or (A cytosolic p65 /A GAPDH ) ×100%, or (A nuclear p65 /A histone 3 ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. IL, interleukin; IgG, immunoglobulin G; TPCA-1,10, thiophene-3-carbox-amide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe; NF-κB, nuclear factor-κB; IκBα, inhibitor of kappa B alpha.

    Techniques Used: Activation Assay, Western Blot, Cell Culture, Control, Standard Deviation



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    Image Search Results


    OAA suppressed infiltration of immune cells and macrophages in the spinal cords of EAE mice. H&E staining showed that OAA administration attenuated inflammatory infiltration in spinal cords compared to the infiltration observed in EAE mice (upper panel). Immunohistochemistry showed that infiltration of CD68+ macrophages was reduced in the spinal cords of OAA-treated mice (lower panel). Expression of TLR2 was elevated in EAE spinal cords and mainly expressed in CD68 + macrophages (lower panel). Scale bars = 100 µm. OAA, oleanolic acid acetate; EAE, experimental autoimmune encephalomyelitis; H&E, hematoxylin and eosin.

    Journal: Frontiers in Pharmacology

    Article Title: Oleanolic Acid Acetate Alleviates Symptoms of Experimental Autoimmune Encephalomyelitis in Mice by Regulating Toll-Like Receptor 2 Signaling

    doi: 10.3389/fphar.2020.556391

    Figure Lengend Snippet: OAA suppressed infiltration of immune cells and macrophages in the spinal cords of EAE mice. H&E staining showed that OAA administration attenuated inflammatory infiltration in spinal cords compared to the infiltration observed in EAE mice (upper panel). Immunohistochemistry showed that infiltration of CD68+ macrophages was reduced in the spinal cords of OAA-treated mice (lower panel). Expression of TLR2 was elevated in EAE spinal cords and mainly expressed in CD68 + macrophages (lower panel). Scale bars = 100 µm. OAA, oleanolic acid acetate; EAE, experimental autoimmune encephalomyelitis; H&E, hematoxylin and eosin.

    Article Snippet: The slides were incubated overnight with rabbit polyclonal anti-mouse TLR2 (1:100, Thermo Fisher Scientific Inc., Waltham, MA, USA), and rat monoclonal anti-mouse CD68 (1:100, Thermo Fisher Scientific Inc., Waltham, MA, USA) antibodies at 4°C.

    Techniques: Staining, Immunohistochemistry, Expressing

    OAA downregulated the expression of TLR2 and downstream signaling molecules in the spinal cords of EAE mice. OAA downregulated TLR2 and MyD88 mRNA expression in the spinal cords (A) . Western blot analysis of TLR2, MyD88, IRAK4, and TRAF6 (B) . The expression level of TLR2, MyD88, IRAK4, and TRAF6 was significantly suppressed in OAA treated group, compared with that of EAE group (B) . Data are shown as mean ± standard error (SE), n=6, *p < 0.05 compared to EAE mice. OAA, oleanolic acid acetate; EAE, experimental autoimmune encephalomyelitis; TLR2, Toll-like receptor 2; MyD88, myeloid differentiation primary response protein 88; IRAK4, IL-1 receptor-associated kinase 4: TRAF6, tumor necrosis factor (TNF) receptor-associated factor 6.

    Journal: Frontiers in Pharmacology

    Article Title: Oleanolic Acid Acetate Alleviates Symptoms of Experimental Autoimmune Encephalomyelitis in Mice by Regulating Toll-Like Receptor 2 Signaling

    doi: 10.3389/fphar.2020.556391

    Figure Lengend Snippet: OAA downregulated the expression of TLR2 and downstream signaling molecules in the spinal cords of EAE mice. OAA downregulated TLR2 and MyD88 mRNA expression in the spinal cords (A) . Western blot analysis of TLR2, MyD88, IRAK4, and TRAF6 (B) . The expression level of TLR2, MyD88, IRAK4, and TRAF6 was significantly suppressed in OAA treated group, compared with that of EAE group (B) . Data are shown as mean ± standard error (SE), n=6, *p < 0.05 compared to EAE mice. OAA, oleanolic acid acetate; EAE, experimental autoimmune encephalomyelitis; TLR2, Toll-like receptor 2; MyD88, myeloid differentiation primary response protein 88; IRAK4, IL-1 receptor-associated kinase 4: TRAF6, tumor necrosis factor (TNF) receptor-associated factor 6.

    Article Snippet: The slides were incubated overnight with rabbit polyclonal anti-mouse TLR2 (1:100, Thermo Fisher Scientific Inc., Waltham, MA, USA), and rat monoclonal anti-mouse CD68 (1:100, Thermo Fisher Scientific Inc., Waltham, MA, USA) antibodies at 4°C.

    Techniques: Expressing, Western Blot

    (A–F) Expression of TLR2 in lung tissue from the mice in each group was assessed using immunohistochemistry (deep brown cellular area indicates positive staining; magnification, x200). (G) Quantification of TLR2-positive staining in five fields of view per section from each mouse was assessed by JD-801 computer-aided image analyzer under high-power magnification (x200). Values are expressed as the mean ± standard deviation of five mice in each group. * P<0.05, as compared with the NC group. # P<0.05, as compared with the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit IgG-treated AM; TLR, of toll-like receptor.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: (A–F) Expression of TLR2 in lung tissue from the mice in each group was assessed using immunohistochemistry (deep brown cellular area indicates positive staining; magnification, x200). (G) Quantification of TLR2-positive staining in five fields of view per section from each mouse was assessed by JD-801 computer-aided image analyzer under high-power magnification (x200). Values are expressed as the mean ± standard deviation of five mice in each group. * P<0.05, as compared with the NC group. # P<0.05, as compared with the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit IgG-treated AM; TLR, of toll-like receptor.

    Article Snippet: The blots were incubated with primary rabbit anti-mouse polyclonal antibodies against TLR2 (cat. no. sc-10739), MyD88 (cat. no. sc-11356) or β-actin (cat. no. sc-130656; Santa Cruz Biotechnology, Inc.) at 1:2,000 dilution overnight followed by incubation for 2 h with an HRP-conjugated goat anti-rabbit IgG antibody (Jackson, West Grove, PA, USA) at 1:5,000 dilution.

    Techniques: Expressing, Immunohistochemistry, Staining, Standard Deviation, Control

    Expressions of TLR2 and MyD88 assessed using western blot analysis in lung tissue obtained from the mice in each group. The western blot shown is a representative of five independent experiments, and β-actin protein served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) × 100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as mean ± standard deviation of five mice in each group. * P<0.05, as compared with the arbitrary units of the same protein in the NC group. # P<0.05, as compared with the arbitrary units of the same protein in the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit immunoglobulin G-treated AM; MyD88, mycloid differentiation factor 88; TLR, toll-like receptor.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: Expressions of TLR2 and MyD88 assessed using western blot analysis in lung tissue obtained from the mice in each group. The western blot shown is a representative of five independent experiments, and β-actin protein served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) × 100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as mean ± standard deviation of five mice in each group. * P<0.05, as compared with the arbitrary units of the same protein in the NC group. # P<0.05, as compared with the arbitrary units of the same protein in the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit immunoglobulin G-treated AM; MyD88, mycloid differentiation factor 88; TLR, toll-like receptor.

    Article Snippet: The blots were incubated with primary rabbit anti-mouse polyclonal antibodies against TLR2 (cat. no. sc-10739), MyD88 (cat. no. sc-11356) or β-actin (cat. no. sc-130656; Santa Cruz Biotechnology, Inc.) at 1:2,000 dilution overnight followed by incubation for 2 h with an HRP-conjugated goat anti-rabbit IgG antibody (Jackson, West Grove, PA, USA) at 1:5,000 dilution.

    Techniques: Western Blot, Control, Standard Deviation

    Supernatant levels of IL-4, IL-6 and IL-8 released from leukocytes exposed to IL-1β were assessed using ELISA. The cultured leukocytes were obtained from a mouse from the normal control group and stimulated with IL-1β (10 ng/ml) for 24 h with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h and TPCA-1 (10 μ M) for 1 h. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the levels of same cytokine released from the cells without treatment. # P<0.05, as compared to the levels of same cytokine released from the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin G; TLR, toll-like receptor; TPCA-1,10, thiophene-3-carboxamide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: Supernatant levels of IL-4, IL-6 and IL-8 released from leukocytes exposed to IL-1β were assessed using ELISA. The cultured leukocytes were obtained from a mouse from the normal control group and stimulated with IL-1β (10 ng/ml) for 24 h with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h and TPCA-1 (10 μ M) for 1 h. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the levels of same cytokine released from the cells without treatment. # P<0.05, as compared to the levels of same cytokine released from the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin G; TLR, toll-like receptor; TPCA-1,10, thiophene-3-carboxamide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Article Snippet: The blots were incubated with primary rabbit anti-mouse polyclonal antibodies against TLR2 (cat. no. sc-10739), MyD88 (cat. no. sc-11356) or β-actin (cat. no. sc-130656; Santa Cruz Biotechnology, Inc.) at 1:2,000 dilution overnight followed by incubation for 2 h with an HRP-conjugated goat anti-rabbit IgG antibody (Jackson, West Grove, PA, USA) at 1:5,000 dilution.

    Techniques: Enzyme-linked Immunosorbent Assay, Cell Culture, Control, Standard Deviation

    Expression of TLR2 and MyD88 assessed using western blot analysis of leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 30 min with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h and MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h. The western blot is representative of five independent experiments, and the lower panel shows β-actin protein, which served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) ×100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. # P<0.05, as compared to the arbitrary units of the same protein in the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin; TLR, toll-like receptor; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: Expression of TLR2 and MyD88 assessed using western blot analysis of leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 30 min with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h and MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h. The western blot is representative of five independent experiments, and the lower panel shows β-actin protein, which served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) ×100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. # P<0.05, as compared to the arbitrary units of the same protein in the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin; TLR, toll-like receptor; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Article Snippet: The blots were incubated with primary rabbit anti-mouse polyclonal antibodies against TLR2 (cat. no. sc-10739), MyD88 (cat. no. sc-11356) or β-actin (cat. no. sc-130656; Santa Cruz Biotechnology, Inc.) at 1:2,000 dilution overnight followed by incubation for 2 h with an HRP-conjugated goat anti-rabbit IgG antibody (Jackson, West Grove, PA, USA) at 1:5,000 dilution.

    Techniques: Expressing, Western Blot, Cell Culture, Control, Standard Deviation

    Activation of NF-κB assessed using western blot analysis in leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 1 h with or without pre-treatment of BML-111 (1 mM) for 30 min, BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, ST2825 (20 μ M) for 1 h or TPCA-1 (10 μ M) for 1 h. The western blot is representative of five independent experiments. GAPDH served as a loading control of cytosolic proteins. Histone 3 protein served as a loading control of nuclear proteins. Semiquantitative analysis was performed using UVP-gel densitometry. Arbitrary unit = (A IκBα /A GAPDH ) ×100%, or (A cytosolic p65 /A GAPDH ) ×100%, or (A nuclear p65 /A histone 3 ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. IL, interleukin; IgG, immunoglobulin G; TPCA-1,10, thiophene-3-carbox-amide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe; NF-κB, nuclear factor-κB; IκBα, inhibitor of kappa B alpha.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: Activation of NF-κB assessed using western blot analysis in leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 1 h with or without pre-treatment of BML-111 (1 mM) for 30 min, BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, ST2825 (20 μ M) for 1 h or TPCA-1 (10 μ M) for 1 h. The western blot is representative of five independent experiments. GAPDH served as a loading control of cytosolic proteins. Histone 3 protein served as a loading control of nuclear proteins. Semiquantitative analysis was performed using UVP-gel densitometry. Arbitrary unit = (A IκBα /A GAPDH ) ×100%, or (A cytosolic p65 /A GAPDH ) ×100%, or (A nuclear p65 /A histone 3 ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. IL, interleukin; IgG, immunoglobulin G; TPCA-1,10, thiophene-3-carbox-amide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe; NF-κB, nuclear factor-κB; IκBα, inhibitor of kappa B alpha.

    Article Snippet: The blots were incubated with primary rabbit anti-mouse polyclonal antibodies against TLR2 (cat. no. sc-10739), MyD88 (cat. no. sc-11356) or β-actin (cat. no. sc-130656; Santa Cruz Biotechnology, Inc.) at 1:2,000 dilution overnight followed by incubation for 2 h with an HRP-conjugated goat anti-rabbit IgG antibody (Jackson, West Grove, PA, USA) at 1:5,000 dilution.

    Techniques: Activation Assay, Western Blot, Cell Culture, Control, Standard Deviation

    (A–F) Expression of TLR2 in lung tissue from the mice in each group was assessed using immunohistochemistry (deep brown cellular area indicates positive staining; magnification, x200). (G) Quantification of TLR2-positive staining in five fields of view per section from each mouse was assessed by JD-801 computer-aided image analyzer under high-power magnification (x200). Values are expressed as the mean ± standard deviation of five mice in each group. * P<0.05, as compared with the NC group. # P<0.05, as compared with the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit IgG-treated AM; TLR, of toll-like receptor.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: (A–F) Expression of TLR2 in lung tissue from the mice in each group was assessed using immunohistochemistry (deep brown cellular area indicates positive staining; magnification, x200). (G) Quantification of TLR2-positive staining in five fields of view per section from each mouse was assessed by JD-801 computer-aided image analyzer under high-power magnification (x200). Values are expressed as the mean ± standard deviation of five mice in each group. * P<0.05, as compared with the NC group. # P<0.05, as compared with the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit IgG-treated AM; TLR, of toll-like receptor.

    Article Snippet: Sections were incubated with either rabbit anti-mouse polyclonal TLR2 antibody (cat. no. sc-10739) or rabbit anti-mouse polyclonal phosphorylated NF-κB p65 (Ser 276) antibody (cat. no. sc-109; Santa Cruz Biotechnology, Inc.) at 1:100 dilution.

    Techniques: Expressing, Immunohistochemistry, Staining, Standard Deviation, Control

    Expressions of TLR2 and MyD88 assessed using western blot analysis in lung tissue obtained from the mice in each group. The western blot shown is a representative of five independent experiments, and β-actin protein served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) × 100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as mean ± standard deviation of five mice in each group. * P<0.05, as compared with the arbitrary units of the same protein in the NC group. # P<0.05, as compared with the arbitrary units of the same protein in the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit immunoglobulin G-treated AM; MyD88, mycloid differentiation factor 88; TLR, toll-like receptor.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: Expressions of TLR2 and MyD88 assessed using western blot analysis in lung tissue obtained from the mice in each group. The western blot shown is a representative of five independent experiments, and β-actin protein served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) × 100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as mean ± standard deviation of five mice in each group. * P<0.05, as compared with the arbitrary units of the same protein in the NC group. # P<0.05, as compared with the arbitrary units of the same protein in the AM group. NC, normal control; AM, ovalbumin immunization-induced asthmatic mice; BAM, BML-111-treated AM; VAM, vehicle of BML-111-treated AM; AAM, anti-IL-1β antibody-treated AM; RAM, rabbit immunoglobulin G-treated AM; MyD88, mycloid differentiation factor 88; TLR, toll-like receptor.

    Article Snippet: Sections were incubated with either rabbit anti-mouse polyclonal TLR2 antibody (cat. no. sc-10739) or rabbit anti-mouse polyclonal phosphorylated NF-κB p65 (Ser 276) antibody (cat. no. sc-109; Santa Cruz Biotechnology, Inc.) at 1:100 dilution.

    Techniques: Western Blot, Control, Standard Deviation

    Supernatant levels of IL-4, IL-6 and IL-8 released from leukocytes exposed to IL-1β were assessed using ELISA. The cultured leukocytes were obtained from a mouse from the normal control group and stimulated with IL-1β (10 ng/ml) for 24 h with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h and TPCA-1 (10 μ M) for 1 h. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the levels of same cytokine released from the cells without treatment. # P<0.05, as compared to the levels of same cytokine released from the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin G; TLR, toll-like receptor; TPCA-1,10, thiophene-3-carboxamide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: Supernatant levels of IL-4, IL-6 and IL-8 released from leukocytes exposed to IL-1β were assessed using ELISA. The cultured leukocytes were obtained from a mouse from the normal control group and stimulated with IL-1β (10 ng/ml) for 24 h with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h and TPCA-1 (10 μ M) for 1 h. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the levels of same cytokine released from the cells without treatment. # P<0.05, as compared to the levels of same cytokine released from the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin G; TLR, toll-like receptor; TPCA-1,10, thiophene-3-carboxamide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Article Snippet: Sections were incubated with either rabbit anti-mouse polyclonal TLR2 antibody (cat. no. sc-10739) or rabbit anti-mouse polyclonal phosphorylated NF-κB p65 (Ser 276) antibody (cat. no. sc-109; Santa Cruz Biotechnology, Inc.) at 1:100 dilution.

    Techniques: Enzyme-linked Immunosorbent Assay, Cell Culture, Control, Standard Deviation

    Expression of TLR2 and MyD88 assessed using western blot analysis of leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 30 min with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h and MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h. The western blot is representative of five independent experiments, and the lower panel shows β-actin protein, which served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) ×100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. # P<0.05, as compared to the arbitrary units of the same protein in the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin; TLR, toll-like receptor; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: Expression of TLR2 and MyD88 assessed using western blot analysis of leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 30 min with or without pre-treatment of BML-111 (1 mM) for 30 min, antagonist of G protein-coupled LXA4 receptor BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h and MyD88 dimerization inhibitor ST2825 (20 μ M) for 1 h. The western blot is representative of five independent experiments, and the lower panel shows β-actin protein, which served as a loading control. Semiquantitative analysis was performed by using UVP-gel densitometry. Arbitrary unit = (A TLR2 /A β-actin ) ×100%, or (A MyD88 /A β-actin ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. # P<0.05, as compared to the arbitrary units of the same protein in the cells treated with IL-1β alone. IL, interleukin; IgG, immunoglobulin; TLR, toll-like receptor; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe.

    Article Snippet: Sections were incubated with either rabbit anti-mouse polyclonal TLR2 antibody (cat. no. sc-10739) or rabbit anti-mouse polyclonal phosphorylated NF-κB p65 (Ser 276) antibody (cat. no. sc-109; Santa Cruz Biotechnology, Inc.) at 1:100 dilution.

    Techniques: Expressing, Western Blot, Cell Culture, Control, Standard Deviation

    Activation of NF-κB assessed using western blot analysis in leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 1 h with or without pre-treatment of BML-111 (1 mM) for 30 min, BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, ST2825 (20 μ M) for 1 h or TPCA-1 (10 μ M) for 1 h. The western blot is representative of five independent experiments. GAPDH served as a loading control of cytosolic proteins. Histone 3 protein served as a loading control of nuclear proteins. Semiquantitative analysis was performed using UVP-gel densitometry. Arbitrary unit = (A IκBα /A GAPDH ) ×100%, or (A cytosolic p65 /A GAPDH ) ×100%, or (A nuclear p65 /A histone 3 ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. IL, interleukin; IgG, immunoglobulin G; TPCA-1,10, thiophene-3-carbox-amide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe; NF-κB, nuclear factor-κB; IκBα, inhibitor of kappa B alpha.

    Journal: Molecular Medicine Reports

    Article Title: Roles of lipoxin A4 receptor activation and anti-interleukin-1β antibody on the toll-like receptor 2/mycloid differentiation factor 88/nuclear factor-κB pathway in airway inflammation induced by ovalbumin

    doi: 10.3892/mmr.2015.3443

    Figure Lengend Snippet: Activation of NF-κB assessed using western blot analysis in leukocytes exposed to IL-1β. The cultured leukocytes were obtained from a normal control mouse and stimulated with IL-1β (10 ng/ml) for 1 h with or without pre-treatment of BML-111 (1 mM) for 30 min, BOC1 (100 μ M) for 30 min, TLR2Ab (1 μ g/ml) for 1 h, goat IgG (1 μ g/ml) for 1 h, ST2825 (20 μ M) for 1 h or TPCA-1 (10 μ M) for 1 h. The western blot is representative of five independent experiments. GAPDH served as a loading control of cytosolic proteins. Histone 3 protein served as a loading control of nuclear proteins. Semiquantitative analysis was performed using UVP-gel densitometry. Arbitrary unit = (A IκBα /A GAPDH ) ×100%, or (A cytosolic p65 /A GAPDH ) ×100%, or (A nuclear p65 /A histone 3 ) ×100%. Values are expressed as the mean ± standard deviation of five independent experiments. * P<0.05, as compared to the arbitrary units of the same protein in the cells without treatment. IL, interleukin; IgG, immunoglobulin G; TPCA-1,10, thiophene-3-carbox-amide 1; TLR2Ab, toll-like receptor 2-neutralizing antibody; BOC1, N -t-Boc-Phe-Leu-Phe-Leu-Phe; NF-κB, nuclear factor-κB; IκBα, inhibitor of kappa B alpha.

    Article Snippet: Sections were incubated with either rabbit anti-mouse polyclonal TLR2 antibody (cat. no. sc-10739) or rabbit anti-mouse polyclonal phosphorylated NF-κB p65 (Ser 276) antibody (cat. no. sc-109; Santa Cruz Biotechnology, Inc.) at 1:100 dilution.

    Techniques: Activation Assay, Western Blot, Cell Culture, Control, Standard Deviation