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Bioworld Antibodies rabbit monoclonal antibody against nf κb p65
Effects of artemisinin on the nuclear translocation of nuclear factor‐kappa B <t>(NF‐κB)</t> <t>p65</t> in APPswe/PS1dE9 double transgenic mice. Brain tissues from APPswe/PS1dE9 mice were subjected to immunohistochemistry to determine the nuclear translocation of NF‐κB p65. (A) Representative photographs of immunohistochemistry <t>staining</t> <t>with</t> <t>anti‐NF‐κB</t> p65 antibody (with 200× magnification). (B) Representative photographs of immunohistochemistry staining with anti‐NF‐κB p65 antibody (with 400× magnification). Artemisinin significantly reduced the ratio of NF‐κB p65 nuclear–positive cells. Black arrows point to NF‐κB p65 nuclear–positive cells. Bars: 50 μm. (C) Quantification of the ratio of NF‐κB p65 nuclear–positive cells in APPswe/PS1dE9 mice in each group; the numbers represent the mean ± SEM. n = 3 mice each. *P < 0.05 by Student's t‐test.
Rabbit Monoclonal Antibody Against Nf κb P65, supplied by Bioworld Antibodies, 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/product/rabbit+anti+phospho+i%CE%BAb%CE%B1/pmc06493386-109-68-75?v=Bioworld+Antibodies
Average 90 stars, based on 1 article reviews
rabbit monoclonal antibody against nf κb p65 - by Bioz Stars, 2026-07
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Effects of artemisinin on the nuclear translocation of nuclear factor‐kappa B (NF‐κB) p65 in APPswe/PS1dE9 double transgenic mice. Brain tissues from APPswe/PS1dE9 mice were subjected to immunohistochemistry to determine the nuclear translocation of NF‐κB p65. (A) Representative photographs of immunohistochemistry staining with anti‐NF‐κB p65 antibody (with 200× magnification). (B) Representative photographs of immunohistochemistry staining with anti‐NF‐κB p65 antibody (with 400× magnification). Artemisinin significantly reduced the ratio of NF‐κB p65 nuclear–positive cells. Black arrows point to NF‐κB p65 nuclear–positive cells. Bars: 50 μm. (C) Quantification of the ratio of NF‐κB p65 nuclear–positive cells in APPswe/PS1dE9 mice in each group; the numbers represent the mean ± SEM. n = 3 mice each. *P < 0.05 by Student's t‐test.

Journal: CNS Neuroscience & Therapeutics

Article Title: Antimalarial Drug Artemisinin Extenuates Amyloidogenesis and Neuroinflammation in APP swe/ PS 1dE9 Transgenic Mice via Inhibition of Nuclear Factor‐κ B and NLRP 3 Inflammasome Activation

doi: 10.1111/cns.12066

Figure Lengend Snippet: Effects of artemisinin on the nuclear translocation of nuclear factor‐kappa B (NF‐κB) p65 in APPswe/PS1dE9 double transgenic mice. Brain tissues from APPswe/PS1dE9 mice were subjected to immunohistochemistry to determine the nuclear translocation of NF‐κB p65. (A) Representative photographs of immunohistochemistry staining with anti‐NF‐κB p65 antibody (with 200× magnification). (B) Representative photographs of immunohistochemistry staining with anti‐NF‐κB p65 antibody (with 400× magnification). Artemisinin significantly reduced the ratio of NF‐κB p65 nuclear–positive cells. Black arrows point to NF‐κB p65 nuclear–positive cells. Bars: 50 μm. (C) Quantification of the ratio of NF‐κB p65 nuclear–positive cells in APPswe/PS1dE9 mice in each group; the numbers represent the mean ± SEM. n = 3 mice each. *P < 0.05 by Student's t‐test.

Article Snippet: The following primary antibodies were used: mouse anti‐LRP1 antibody [5A6] (1:3000; Merck, Darmstadt, Germany), rabbit anti‐RAGE antibody (1:1000; Cell Signaling, Denver, MA, USA), rabbit anti‐APP carboxyl terminal antibody (1:4000; Sigma), rabbit anti‐BACE1 antibody (1:1000; Cell Signaling), rabbit anti‐PS1 antibody (1:1000; Cell Signaling), rabbit anti‐Aph‐1a antibody (1:3000; Invitrogen, Camarillo, CA, USA), rabbit polyclonal antibody against serine 536 phosphorylated NF‐κB p65 (1: 800; Santa Cruz Biotechnology, Santa Cruz, CA, USA), rabbit monoclonal antibody against NF‐κB p65 (1:500; Bioworld Technology), rabbit anti‐IκB‐α antibody (1:1000; Bioworld Technology), rabbit polyclonal antibody against serine 32 phosphorylated IκB‐α (1:1000; Bioworld Technology), rabbit anti‐NALP3 antibody (1:800; Santa Cruz), rabbit anticleaved caspase‐1 (Asp297) (D57A2) antibody (1:1000; Cell Signaling), and mouse anti‐β‐actin antibody (1:1000; Santa Cruz).

Techniques: Translocation Assay, Transgenic Assay, Immunohistochemistry, Staining

Effect of artemisinin on nuclear factor‐kappa B (NF‐κB) activity in APPswe/PS1dE9 double transgenic mice. (A) Brain tissues from APPswe/PS1dE9 mice were subjected to Western blotting to determine the levels of p‐NF‐κB p65, NF‐κB p65, I‐κBα, and p‐I‐κBα, with β‐actin as a loading control. (B) Quantification of p‐NF‐κB p65, NF‐κB p65, I‐κBα, and p‐I‐κBα. Artemisinin significantly decreased the levels of p‐NF‐κB p65, NF‐κB p65, and p‐I‐κBα and increased the level of I‐κBα. n = 3. *, P < 0.05 by Student's t‐test. (C) An ELISA was conducted to measure brain IL‐6 and TNF‐α level in the brains of mice in each group. Artemisinin significantly reduced IL‐6 and TNF‐α level in brains. n = 3. *, P < 0.05 by Student's t‐test.

Journal: CNS Neuroscience & Therapeutics

Article Title: Antimalarial Drug Artemisinin Extenuates Amyloidogenesis and Neuroinflammation in APP swe/ PS 1dE9 Transgenic Mice via Inhibition of Nuclear Factor‐κ B and NLRP 3 Inflammasome Activation

doi: 10.1111/cns.12066

Figure Lengend Snippet: Effect of artemisinin on nuclear factor‐kappa B (NF‐κB) activity in APPswe/PS1dE9 double transgenic mice. (A) Brain tissues from APPswe/PS1dE9 mice were subjected to Western blotting to determine the levels of p‐NF‐κB p65, NF‐κB p65, I‐κBα, and p‐I‐κBα, with β‐actin as a loading control. (B) Quantification of p‐NF‐κB p65, NF‐κB p65, I‐κBα, and p‐I‐κBα. Artemisinin significantly decreased the levels of p‐NF‐κB p65, NF‐κB p65, and p‐I‐κBα and increased the level of I‐κBα. n = 3. *, P < 0.05 by Student's t‐test. (C) An ELISA was conducted to measure brain IL‐6 and TNF‐α level in the brains of mice in each group. Artemisinin significantly reduced IL‐6 and TNF‐α level in brains. n = 3. *, P < 0.05 by Student's t‐test.

Article Snippet: The following primary antibodies were used: mouse anti‐LRP1 antibody [5A6] (1:3000; Merck, Darmstadt, Germany), rabbit anti‐RAGE antibody (1:1000; Cell Signaling, Denver, MA, USA), rabbit anti‐APP carboxyl terminal antibody (1:4000; Sigma), rabbit anti‐BACE1 antibody (1:1000; Cell Signaling), rabbit anti‐PS1 antibody (1:1000; Cell Signaling), rabbit anti‐Aph‐1a antibody (1:3000; Invitrogen, Camarillo, CA, USA), rabbit polyclonal antibody against serine 536 phosphorylated NF‐κB p65 (1: 800; Santa Cruz Biotechnology, Santa Cruz, CA, USA), rabbit monoclonal antibody against NF‐κB p65 (1:500; Bioworld Technology), rabbit anti‐IκB‐α antibody (1:1000; Bioworld Technology), rabbit polyclonal antibody against serine 32 phosphorylated IκB‐α (1:1000; Bioworld Technology), rabbit anti‐NALP3 antibody (1:800; Santa Cruz), rabbit anticleaved caspase‐1 (Asp297) (D57A2) antibody (1:1000; Cell Signaling), and mouse anti‐β‐actin antibody (1:1000; Santa Cruz).

Techniques: Activity Assay, Transgenic Assay, Western Blot, Enzyme-linked Immunosorbent Assay