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Merck KGaA rabbit anti-mouse tlr2 polyclonal antibody
Rabbit Anti Mouse Tlr2 Polyclonal Antibody, supplied by Merck KGaA, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti-mouse tlr2 polyclonal antibody/product/Merck KGaA
Average 90 stars, based on 1 article reviews
rabbit anti-mouse tlr2 polyclonal antibody - by Bioz Stars, 2026-02
90/100 stars

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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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 96 stars, based on 1 article reviews
rabbit anti mouse polyclonal antibodies against tlr2 - by Bioz Stars, 2026-02
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Santa Cruz Biotechnology rabbit anti mouse polyclonal tlr2 antibody
(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.
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https://www.bioz.com/result/rabbit anti mouse polyclonal tlr2 antibody/product/Santa Cruz Biotechnology
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Novus Biologicals rabbit anti-mouse tlr2 polyclonal antibody
(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 Tlr2 Polyclonal Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews
rabbit anti-mouse tlr2 polyclonal antibody - by Bioz Stars, 2026-02
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(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