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Primers used for qRT-PCR.
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XPJYF treatment targeted astrocyte activation and glucose metabolism. (A) Uptake of 2DGP in astrocyte. (B) Glucose‐1‐phosphate level in astrocyte. (C) ATP content. (D) Western blotting. (E) The relative expression of <t>COX‐2</t> in astrocyte. (F) IL‐6 expression in astrocyte. (G) TNF‐α expression in astrocyte. (H) iNOS expression in astrocyte. (I) IL‐1 expression in astrocyte. (J) BDNF expression in astrocyte. (K) Astrocyte activation by GFAP immunofluorescence.
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XPJYF treatment targeted astrocyte activation and glucose metabolism. (A) Uptake of 2DGP in astrocyte. (B) Glucose‐1‐phosphate level in astrocyte. (C) ATP content. (D) Western blotting. (E) The relative expression of <t>COX‐2</t> in astrocyte. (F) IL‐6 expression in astrocyte. (G) TNF‐α expression in astrocyte. (H) iNOS expression in astrocyte. (I) IL‐1 expression in astrocyte. (J) BDNF expression in astrocyte. (K) Astrocyte activation by GFAP immunofluorescence.
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Ferroptosis plays an important role in S100-induced autoimmune hepatitis. (a) Experimental protocol for the modeling of S100-induced AIH model mice. (b)–(d) The serum ALT, AST, and IgG expression levels in the control and AIH groups. (e) Representative H&E staining of liver tissue sections. The black arrow indicates lymphocytic infiltration (original magnification 20×). (f) TNF- α , IFN γ , IL-17, IL-10, and TGF- β levels in liver. (g) IHC staining of <t>COX2</t> and GPX4 in liver sections (original magnification 20×). (h) Semiquantitative IHC results. (i)–(j) Western blotting showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the pre-experimental control and AIH groups. GAPDH was used as a loading control; ∗ P < 0.05, compared with the control group.
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IHC staining for Wnt5a (A–D; ×400); IHC staining for JNK1 (E–H; ×400); IHC staining for NF-κB p65 (I–L; ×400); IHC staining for <t>COX-2</t> (M–P; ×400). The Integral Optical Density(IOD) of Wnt5a (Q), JNK1 (R), NF-κB p65 (S); COX-2 (T). * P <0.01 vs. the control group and the control-cele group; ** P <0.01 vs. the T2DM-NASH group. White = control; Gray = control-cele; Black = T2DM-NASH; Striped = T2DM-NASH-Cele.
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Effects of CPhGs on the expression of <t>COX‐2</t> and HMGB‐1 proteins in myocardial tissues of rats after AAC. (a) <t>Cyclooxygenase</t> <t>2</t> (COX‐2) and (b) high mobility group protein B1 (HMGB‐1). ∗∗ P < 0.01 versus sham. # P < 0.05. ## P < 0.01 versus AAC. Δ P < 0.05, ΔΔ P < 0.01 versus AV ( n = 6).
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Image Search Results


Primers used for qRT-PCR.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Honokiol Ameliorates DSS-Induced Mouse Colitis by Inhibiting Inflammation and Oxidative Stress and Improving the Intestinal Barrier

doi: 10.1155/2022/1755608

Figure Lengend Snippet: Primers used for qRT-PCR.

Article Snippet: After blocking the PVDF membranes with 5% skim milk (Solarbio, China) for one hour at room temperature, washed with Tris-buffered saline Tween (TBST) solution twice, the membranes were incubated with the primary antibodies (NF- κ B p65 (Proteintech, USA), NRF2 (Proteintech, USA), HO1 (Proteintech, USA), phosphorylation-AMPK α (Thr172) (Cell Signaling, USA), AMPK (Proteintech, USA), SIRT3 (Proteintech, USA), COX2 (Proteintech, USA), iNOS (Proteintech, USA), ZO1 (Proteintech, USA), occludin (Proteintech, USA), Claudin1 (Proteintech, USA), and GAPDH (Proteintech, USA) (dilution 1 : 1000)) overnight at 4°C and washed with TBST thrice, followed by incubation with an HRP-conjugated anti-mouse or anti-rabbit secondary antibody (ABclonal, USA) (dilution 1 : 2000) at room temperature for one hour and rinsed thrice with TBST buffer.

Techniques: Sequencing

HKL treatment decreases inflammatory mediators in DSS-induced mice. The levels of (a) IL-1 β , (b) IL-6, (c) TNF- α , (d) iNOS, and (e) COX2 mRNA were measured by qRT-PCR analyses. Data are expressed as mean ± SEM ( n = 3). ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Honokiol Ameliorates DSS-Induced Mouse Colitis by Inhibiting Inflammation and Oxidative Stress and Improving the Intestinal Barrier

doi: 10.1155/2022/1755608

Figure Lengend Snippet: HKL treatment decreases inflammatory mediators in DSS-induced mice. The levels of (a) IL-1 β , (b) IL-6, (c) TNF- α , (d) iNOS, and (e) COX2 mRNA were measured by qRT-PCR analyses. Data are expressed as mean ± SEM ( n = 3). ∗∗ P < 0.01, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

Article Snippet: After blocking the PVDF membranes with 5% skim milk (Solarbio, China) for one hour at room temperature, washed with Tris-buffered saline Tween (TBST) solution twice, the membranes were incubated with the primary antibodies (NF- κ B p65 (Proteintech, USA), NRF2 (Proteintech, USA), HO1 (Proteintech, USA), phosphorylation-AMPK α (Thr172) (Cell Signaling, USA), AMPK (Proteintech, USA), SIRT3 (Proteintech, USA), COX2 (Proteintech, USA), iNOS (Proteintech, USA), ZO1 (Proteintech, USA), occludin (Proteintech, USA), Claudin1 (Proteintech, USA), and GAPDH (Proteintech, USA) (dilution 1 : 1000)) overnight at 4°C and washed with TBST thrice, followed by incubation with an HRP-conjugated anti-mouse or anti-rabbit secondary antibody (ABclonal, USA) (dilution 1 : 2000) at room temperature for one hour and rinsed thrice with TBST buffer.

Techniques: Quantitative RT-PCR

HKL suppressed proinflammatory cytokine expression in LPS-stimulated macrophages. (a) CCK-8 analyzed the effects of HKL at different concentrations on the viability of RAW264.7 cells and MCEC. (b) RAW 264.7 cells were pretreated with 10 μ M HKL for one hour and then stimulated with LPS (1 μ g/ml) for 6 hours. QRT-PCR analyses of the mRNA expression of IL-1 β , IL-6, and TNF- α were measured. mRNA expression was normalized to β -actin expression. (c) RAW 264.7 cells were pretreated with 10 μ M HKL for one hour and then stimulated with LPS (1 μ g/ml) for 12 h. Western blots and related quantification of iNOS and COX2 expressed as a percent of control. Data are expressed as mean ± SEM ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: Honokiol Ameliorates DSS-Induced Mouse Colitis by Inhibiting Inflammation and Oxidative Stress and Improving the Intestinal Barrier

doi: 10.1155/2022/1755608

Figure Lengend Snippet: HKL suppressed proinflammatory cytokine expression in LPS-stimulated macrophages. (a) CCK-8 analyzed the effects of HKL at different concentrations on the viability of RAW264.7 cells and MCEC. (b) RAW 264.7 cells were pretreated with 10 μ M HKL for one hour and then stimulated with LPS (1 μ g/ml) for 6 hours. QRT-PCR analyses of the mRNA expression of IL-1 β , IL-6, and TNF- α were measured. mRNA expression was normalized to β -actin expression. (c) RAW 264.7 cells were pretreated with 10 μ M HKL for one hour and then stimulated with LPS (1 μ g/ml) for 12 h. Western blots and related quantification of iNOS and COX2 expressed as a percent of control. Data are expressed as mean ± SEM ( n = 3). ∗ P < 0.05, ∗∗∗ P < 0.001, and ∗∗∗∗ P < 0.0001.

Article Snippet: After blocking the PVDF membranes with 5% skim milk (Solarbio, China) for one hour at room temperature, washed with Tris-buffered saline Tween (TBST) solution twice, the membranes were incubated with the primary antibodies (NF- κ B p65 (Proteintech, USA), NRF2 (Proteintech, USA), HO1 (Proteintech, USA), phosphorylation-AMPK α (Thr172) (Cell Signaling, USA), AMPK (Proteintech, USA), SIRT3 (Proteintech, USA), COX2 (Proteintech, USA), iNOS (Proteintech, USA), ZO1 (Proteintech, USA), occludin (Proteintech, USA), Claudin1 (Proteintech, USA), and GAPDH (Proteintech, USA) (dilution 1 : 1000)) overnight at 4°C and washed with TBST thrice, followed by incubation with an HRP-conjugated anti-mouse or anti-rabbit secondary antibody (ABclonal, USA) (dilution 1 : 2000) at room temperature for one hour and rinsed thrice with TBST buffer.

Techniques: Expressing, CCK-8 Assay, Quantitative RT-PCR, Western Blot

XPJYF treatment targeted astrocyte activation and glucose metabolism. (A) Uptake of 2DGP in astrocyte. (B) Glucose‐1‐phosphate level in astrocyte. (C) ATP content. (D) Western blotting. (E) The relative expression of COX‐2 in astrocyte. (F) IL‐6 expression in astrocyte. (G) TNF‐α expression in astrocyte. (H) iNOS expression in astrocyte. (I) IL‐1 expression in astrocyte. (J) BDNF expression in astrocyte. (K) Astrocyte activation by GFAP immunofluorescence.

Journal: CNS Neuroscience & Therapeutics

Article Title: Antidepression of Xingpijieyu formula targets gut microbiota derived from depressive disorder

doi: 10.1111/cns.14049

Figure Lengend Snippet: XPJYF treatment targeted astrocyte activation and glucose metabolism. (A) Uptake of 2DGP in astrocyte. (B) Glucose‐1‐phosphate level in astrocyte. (C) ATP content. (D) Western blotting. (E) The relative expression of COX‐2 in astrocyte. (F) IL‐6 expression in astrocyte. (G) TNF‐α expression in astrocyte. (H) iNOS expression in astrocyte. (I) IL‐1 expression in astrocyte. (J) BDNF expression in astrocyte. (K) Astrocyte activation by GFAP immunofluorescence.

Article Snippet: Membranes were incubated with anti‐TNF‐α (1/1000, 17590‐1‐AP, Proteintech, Wuhan, China), interleukin‐1β (IL‐1β) (1/1000, 12242s, Cell Signaling Technology, USA), IL‐6 (1/1000, 21865‐1‐AP, Proteintech), cyclooxygenase‐2 (COX‐2) (1/1000, 12375‐1‐AP, Proteintech), inducible nitric oxide synthase (iNOS) (1/1000, 18985‐1‐AP, Proteintech), and BDNF (1/1000, 28205‐1‐AP, Proteintech) overnight at 4°C, respectively.

Techniques: Activation Assay, Western Blot, Expressing, Immunofluorescence

Ferroptosis plays an important role in S100-induced autoimmune hepatitis. (a) Experimental protocol for the modeling of S100-induced AIH model mice. (b)–(d) The serum ALT, AST, and IgG expression levels in the control and AIH groups. (e) Representative H&E staining of liver tissue sections. The black arrow indicates lymphocytic infiltration (original magnification 20×). (f) TNF- α , IFN γ , IL-17, IL-10, and TGF- β levels in liver. (g) IHC staining of COX2 and GPX4 in liver sections (original magnification 20×). (h) Semiquantitative IHC results. (i)–(j) Western blotting showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the pre-experimental control and AIH groups. GAPDH was used as a loading control; ∗ P < 0.05, compared with the control group.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: GPX4-Regulated Ferroptosis Mediates S100-Induced Experimental Autoimmune Hepatitis Associated with the Nrf2/HO-1 Signaling Pathway

doi: 10.1155/2021/6551069

Figure Lengend Snippet: Ferroptosis plays an important role in S100-induced autoimmune hepatitis. (a) Experimental protocol for the modeling of S100-induced AIH model mice. (b)–(d) The serum ALT, AST, and IgG expression levels in the control and AIH groups. (e) Representative H&E staining of liver tissue sections. The black arrow indicates lymphocytic infiltration (original magnification 20×). (f) TNF- α , IFN γ , IL-17, IL-10, and TGF- β levels in liver. (g) IHC staining of COX2 and GPX4 in liver sections (original magnification 20×). (h) Semiquantitative IHC results. (i)–(j) Western blotting showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the pre-experimental control and AIH groups. GAPDH was used as a loading control; ∗ P < 0.05, compared with the control group.

Article Snippet: The membranes were blocked with 5% skimmed milk in Tris-buffered saline with 0.1% Tween 20 (TBST) and incubated with antibodies against COX2 (1 : 1000, 12375-1-AP, Proteintech), ACSL4 (1 : 1000, A16848, ABclonal), GPX4 (1 : 1000, BM5231, Boster), FTH1 (1 : 1000, A19544, ABclonal), Nrf2 (1 : 1000, 16396-1-AP, Proteintech), HO-1 (1 : 1000, 10701-1-AP, Proteintech), or GAPDH (1 : 10 000, 60004-1-AP, Proteintech) overnight at 4°C.

Techniques: Expressing, Staining, Immunohistochemistry, Western Blot

Ferrostatin-1, a ferroptosis inhibitor, significantly improves S100-induced autoimmune hepatitis. (a) Experimental protocol for Ferrostatin-1 treatment of S100-induced AIH model mice. (b)–(d) ALT, AST, and IgG levels in the control group, AIH group, Ferrostatin-1-treated group, and AIH + Ferrostatin-1 group are shown. (e) Representative H&E staining of liver tissue sections. The black arrow indicates the lymphocytic infiltration (original magnification 20×). (f)TNF- α , IFN γ , IL-17, IL-10, and TGF- β levels in liver; (g) and (h) Western blot showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the control, AIH, Ferrostatin-1, and AIH + Ferrostatin-1 groups; GAPDH was used as a loading control. (i) IHC images of COX2 and GPX4 in liver sections (original magnification 20×). (j) Semiquantitative IHC results. (k) Detection of lipid peroxidation by measuring malondialdehyde (MDA) levels. (l) Fe 2+ levels in liver; ∗ P < 0.05, compared with control group; # P < 0.05, compared with AIH group.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: GPX4-Regulated Ferroptosis Mediates S100-Induced Experimental Autoimmune Hepatitis Associated with the Nrf2/HO-1 Signaling Pathway

doi: 10.1155/2021/6551069

Figure Lengend Snippet: Ferrostatin-1, a ferroptosis inhibitor, significantly improves S100-induced autoimmune hepatitis. (a) Experimental protocol for Ferrostatin-1 treatment of S100-induced AIH model mice. (b)–(d) ALT, AST, and IgG levels in the control group, AIH group, Ferrostatin-1-treated group, and AIH + Ferrostatin-1 group are shown. (e) Representative H&E staining of liver tissue sections. The black arrow indicates the lymphocytic infiltration (original magnification 20×). (f)TNF- α , IFN γ , IL-17, IL-10, and TGF- β levels in liver; (g) and (h) Western blot showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the control, AIH, Ferrostatin-1, and AIH + Ferrostatin-1 groups; GAPDH was used as a loading control. (i) IHC images of COX2 and GPX4 in liver sections (original magnification 20×). (j) Semiquantitative IHC results. (k) Detection of lipid peroxidation by measuring malondialdehyde (MDA) levels. (l) Fe 2+ levels in liver; ∗ P < 0.05, compared with control group; # P < 0.05, compared with AIH group.

Article Snippet: The membranes were blocked with 5% skimmed milk in Tris-buffered saline with 0.1% Tween 20 (TBST) and incubated with antibodies against COX2 (1 : 1000, 12375-1-AP, Proteintech), ACSL4 (1 : 1000, A16848, ABclonal), GPX4 (1 : 1000, BM5231, Boster), FTH1 (1 : 1000, A19544, ABclonal), Nrf2 (1 : 1000, 16396-1-AP, Proteintech), HO-1 (1 : 1000, 10701-1-AP, Proteintech), or GAPDH (1 : 10 000, 60004-1-AP, Proteintech) overnight at 4°C.

Techniques: Staining, Western Blot, Expressing

Exacerbation of S100-induced autoimmune hepatitis after GPX4 knockdown. (a) Experimental protocol for the transfection of AAV8-m-GPX4 and the establishment of the mouse AIH model; (b)–(d) ALT, AST, and IgG levels in the NC + AAV8-m-GPX4, AIH + AAV8-m-GPX4, NC + AAV8-EGFP, and AIH + AAV8-EGFP groups. (e) Representative H&E staining of liver tissue sections. The black arrow indicates lymphocytic infiltration (original magnification 20×); (f) TNF- α , IFN γ , IL-17, IL-10, and TGF- β levels in liver; (g) and (h) Western blot showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the NC + AAV8-m-GPX4, AIH + AAV8-m-GPX4, NC + AAV8-EGFP, and AIH + AAV8-EGFP groups; GAPDH was used as a loading control. (i) IHC images of COX2 and GPX4 in liver sections (original magnification 20×). (j) Semiquantitative IHC results. (k) Detection of lipid peroxidation by measuring malondialdehyde (MDA) levels. (l) Fe 2+ levels in liver; ∗ P < 0.05, compared with the NC + AAV8-EGFP group; # P < 0.05, compared with the AIH + AAV8-EGFP group.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: GPX4-Regulated Ferroptosis Mediates S100-Induced Experimental Autoimmune Hepatitis Associated with the Nrf2/HO-1 Signaling Pathway

doi: 10.1155/2021/6551069

Figure Lengend Snippet: Exacerbation of S100-induced autoimmune hepatitis after GPX4 knockdown. (a) Experimental protocol for the transfection of AAV8-m-GPX4 and the establishment of the mouse AIH model; (b)–(d) ALT, AST, and IgG levels in the NC + AAV8-m-GPX4, AIH + AAV8-m-GPX4, NC + AAV8-EGFP, and AIH + AAV8-EGFP groups. (e) Representative H&E staining of liver tissue sections. The black arrow indicates lymphocytic infiltration (original magnification 20×); (f) TNF- α , IFN γ , IL-17, IL-10, and TGF- β levels in liver; (g) and (h) Western blot showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the NC + AAV8-m-GPX4, AIH + AAV8-m-GPX4, NC + AAV8-EGFP, and AIH + AAV8-EGFP groups; GAPDH was used as a loading control. (i) IHC images of COX2 and GPX4 in liver sections (original magnification 20×). (j) Semiquantitative IHC results. (k) Detection of lipid peroxidation by measuring malondialdehyde (MDA) levels. (l) Fe 2+ levels in liver; ∗ P < 0.05, compared with the NC + AAV8-EGFP group; # P < 0.05, compared with the AIH + AAV8-EGFP group.

Article Snippet: The membranes were blocked with 5% skimmed milk in Tris-buffered saline with 0.1% Tween 20 (TBST) and incubated with antibodies against COX2 (1 : 1000, 12375-1-AP, Proteintech), ACSL4 (1 : 1000, A16848, ABclonal), GPX4 (1 : 1000, BM5231, Boster), FTH1 (1 : 1000, A19544, ABclonal), Nrf2 (1 : 1000, 16396-1-AP, Proteintech), HO-1 (1 : 1000, 10701-1-AP, Proteintech), or GAPDH (1 : 10 000, 60004-1-AP, Proteintech) overnight at 4°C.

Techniques: Transfection, Staining, Western Blot, Expressing

LPS-induced ferroptosis in AML12 cells occurs through the regulation of GPX4. (a) and (b) Western blot showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the control, LPS, Si + LPS, SiNC+LPS, Plasmid+LPS, and PlasmidNC+LPS groups; GAPDH was used as a loading control; (c) and (d) COX2 and GPX4 immunofluorescence detection combined with DAPI staining for nuclei (scale bar: 75 μ m). ∗ P < 0.05, compared with the control group; # P < 0.05, compared with the LPS group.

Journal: Oxidative Medicine and Cellular Longevity

Article Title: GPX4-Regulated Ferroptosis Mediates S100-Induced Experimental Autoimmune Hepatitis Associated with the Nrf2/HO-1 Signaling Pathway

doi: 10.1155/2021/6551069

Figure Lengend Snippet: LPS-induced ferroptosis in AML12 cells occurs through the regulation of GPX4. (a) and (b) Western blot showing protein expression of COX2, ACSL4, GPX4, and FTH1 in the control, LPS, Si + LPS, SiNC+LPS, Plasmid+LPS, and PlasmidNC+LPS groups; GAPDH was used as a loading control; (c) and (d) COX2 and GPX4 immunofluorescence detection combined with DAPI staining for nuclei (scale bar: 75 μ m). ∗ P < 0.05, compared with the control group; # P < 0.05, compared with the LPS group.

Article Snippet: The membranes were blocked with 5% skimmed milk in Tris-buffered saline with 0.1% Tween 20 (TBST) and incubated with antibodies against COX2 (1 : 1000, 12375-1-AP, Proteintech), ACSL4 (1 : 1000, A16848, ABclonal), GPX4 (1 : 1000, BM5231, Boster), FTH1 (1 : 1000, A19544, ABclonal), Nrf2 (1 : 1000, 16396-1-AP, Proteintech), HO-1 (1 : 1000, 10701-1-AP, Proteintech), or GAPDH (1 : 10 000, 60004-1-AP, Proteintech) overnight at 4°C.

Techniques: Western Blot, Expressing, Plasmid Preparation, Immunofluorescence, Staining

IHC staining for Wnt5a (A–D; ×400); IHC staining for JNK1 (E–H; ×400); IHC staining for NF-κB p65 (I–L; ×400); IHC staining for COX-2 (M–P; ×400). The Integral Optical Density(IOD) of Wnt5a (Q), JNK1 (R), NF-κB p65 (S); COX-2 (T). * P <0.01 vs. the control group and the control-cele group; ** P <0.01 vs. the T2DM-NASH group. White = control; Gray = control-cele; Black = T2DM-NASH; Striped = T2DM-NASH-Cele.

Journal: PLoS ONE

Article Title: Celecoxib Ameliorates Non-Alcoholic Steatohepatitis in Type 2 Diabetic Rats via Suppression of the Non-Canonical Wnt Signaling Pathway Expression

doi: 10.1371/journal.pone.0083819

Figure Lengend Snippet: IHC staining for Wnt5a (A–D; ×400); IHC staining for JNK1 (E–H; ×400); IHC staining for NF-κB p65 (I–L; ×400); IHC staining for COX-2 (M–P; ×400). The Integral Optical Density(IOD) of Wnt5a (Q), JNK1 (R), NF-κB p65 (S); COX-2 (T). * P <0.01 vs. the control group and the control-cele group; ** P <0.01 vs. the T2DM-NASH group. White = control; Gray = control-cele; Black = T2DM-NASH; Striped = T2DM-NASH-Cele.

Article Snippet: Proteins were transferred to a PVDF membrane(Thermo Scientific) for 70 min at 100 V. The membranes were incubated in blocking buffer for 2 hours before the addition of primary antibody including Wnt5a (Abcam, USA), JNK1 (Santa Cruz Biotechnology, USA), NF-κB p65 (Abcam, USA) and COX-2 (Proteintech Group, PTG, USA).

Techniques: Immunohistochemistry

Representative western blot images and quantitative analysis of Wnt5a (A), JNK1 p54 and p46 (B), NF-κB p65 (C), and COX-2 (D). GAPDH was used as a loading control. * P <0.01 vs. the control group and the control-cele group; ** P <0.01 vs. the T2DM-NASH group. White = control; Gray = control-cele; Black = T2DM-NASH; Striped = T2DM-NASH-Cele.

Journal: PLoS ONE

Article Title: Celecoxib Ameliorates Non-Alcoholic Steatohepatitis in Type 2 Diabetic Rats via Suppression of the Non-Canonical Wnt Signaling Pathway Expression

doi: 10.1371/journal.pone.0083819

Figure Lengend Snippet: Representative western blot images and quantitative analysis of Wnt5a (A), JNK1 p54 and p46 (B), NF-κB p65 (C), and COX-2 (D). GAPDH was used as a loading control. * P <0.01 vs. the control group and the control-cele group; ** P <0.01 vs. the T2DM-NASH group. White = control; Gray = control-cele; Black = T2DM-NASH; Striped = T2DM-NASH-Cele.

Article Snippet: Proteins were transferred to a PVDF membrane(Thermo Scientific) for 70 min at 100 V. The membranes were incubated in blocking buffer for 2 hours before the addition of primary antibody including Wnt5a (Abcam, USA), JNK1 (Santa Cruz Biotechnology, USA), NF-κB p65 (Abcam, USA) and COX-2 (Proteintech Group, PTG, USA).

Techniques: Western Blot

Quantitative analysis of Wnt5a mRNA (A), NF-κB p65 mRNA (B), COX-2 mRNA (C). β-actin was used as a control. * P <0.01 vs. the control group and the control-cele group; ** P <0.01 vs. the T2DM-NASH group. # P <0.05 vs. the T2DM-NASH group. White = control; Gray = control-cele; Black = T2DM-NASH; Striped = T2DM-NASH-Cele.

Journal: PLoS ONE

Article Title: Celecoxib Ameliorates Non-Alcoholic Steatohepatitis in Type 2 Diabetic Rats via Suppression of the Non-Canonical Wnt Signaling Pathway Expression

doi: 10.1371/journal.pone.0083819

Figure Lengend Snippet: Quantitative analysis of Wnt5a mRNA (A), NF-κB p65 mRNA (B), COX-2 mRNA (C). β-actin was used as a control. * P <0.01 vs. the control group and the control-cele group; ** P <0.01 vs. the T2DM-NASH group. # P <0.05 vs. the T2DM-NASH group. White = control; Gray = control-cele; Black = T2DM-NASH; Striped = T2DM-NASH-Cele.

Article Snippet: Proteins were transferred to a PVDF membrane(Thermo Scientific) for 70 min at 100 V. The membranes were incubated in blocking buffer for 2 hours before the addition of primary antibody including Wnt5a (Abcam, USA), JNK1 (Santa Cruz Biotechnology, USA), NF-κB p65 (Abcam, USA) and COX-2 (Proteintech Group, PTG, USA).

Techniques:

Effects of CPhGs on the expression of COX‐2 and HMGB‐1 proteins in myocardial tissues of rats after AAC. (a) Cyclooxygenase 2 (COX‐2) and (b) high mobility group protein B1 (HMGB‐1). ∗∗ P < 0.01 versus sham. # P < 0.05. ## P < 0.01 versus AAC. Δ P < 0.05, ΔΔ P < 0.01 versus AV ( n = 6).

Journal: Evidence-based Complementary and Alternative Medicine : eCAM

Article Title: Phenylethanol Glycosides Protect Myocardial Hypertrophy Induced by Abdominal Aortic Constriction via ECE-1 Demethylation Inhibition and PI3K/PKB/eNOS Pathway Enhancement

doi: 10.1155/2020/2957094

Figure Lengend Snippet: Effects of CPhGs on the expression of COX‐2 and HMGB‐1 proteins in myocardial tissues of rats after AAC. (a) Cyclooxygenase 2 (COX‐2) and (b) high mobility group protein B1 (HMGB‐1). ∗∗ P < 0.01 versus sham. # P < 0.05. ## P < 0.01 versus AAC. Δ P < 0.05, ΔΔ P < 0.01 versus AV ( n = 6).

Article Snippet: After being blocked with 3% BSA for 2 hours at room temperature, the membranes were incubated with anti-PI3K antibody, anti-phospho-PI3K antibody, anti-eNOS antibody, anti-phospho-eNOS (1 : 1000, Bioss, Beijing, China), anti-COX-2 antibody, anti-HMGB-1 antibody (1 : 1000, Proteintech , Chicago, IL, USA), and anti-ECE-1 antibody (1 : 2000, Signalway Antibody , College Park, MD, USA), primary antibodies overnight at 4°C.

Techniques: Expressing