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tlr2 inhibition (Selleck Chemicals)

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Selleck Chemicals tlr2 inhibition
Tlr2 Inhibition, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cu+cpt22/Cu-CPT22/pm42887494-469-1-4
Average 93 stars, based on 15 article reviews

tlr2 inhibition - by Bioz Stars, 2026-10

93/100 stars

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Control:

Article Title: Tongue sole creatine kinases function as DAMP and activate antimicrobial immunity via TLR2
Article Snippet: .. Tongue sole PBLs were pretreated with DMSO (control) or different concentrations (1 and 10 μM) of CU-CPT22 (TLR2 specific antagonist) (Selleck.cn, Houston, TX, USA) for 2 h, followed by incubation with rCsCKM-1/2 (85 μg/ml), rTrx (85 μg/ml) or PBS for 1 h. After incubation, the expression levels of IL-1β, IL-6 and TNF-α were determined by qRT-PCR as above. .. To examine the effect of CU-CPT22 on phagocytosis, tongue sole PBLs in L-15 medium were settled on 24-well plates (Corning Incorporated, Costar) and treated with CU-CPT22 (10 μM) or DMSO (control) for 2 h. The cells were then incubated with rCsCKM-1/2 (85 μg/ml), rTrx (85 μg/ml) or PBS for 2 h as above.

Incubation:

Expressing:

Quantitative RT-PCR:

In Vivo:

Article Title: SAA1/TLR2 axis directs chemotactic migration of hepatic stellate cells responding to injury
Article Snippet: .. For in vivo inhibition of TLR2 in mice liver, C57BL/6 mice were intraperitoneally injected CU-CPT22, a TLR2 antagonist (Selleck.cn). ..

Inhibition:

Injection:

Article Title: Autophagy Inhibition and Inflammation Activation Induced by Phosphorylated Alpha-synuclein Through Toll-like Receptor 2 Pathway in the Hippocampus of MPTP Mouse Model of Parkinson’s Disease Contribute to Its Cognitive Function Decline in the Early Stage
Article Snippet: .. The saline group was injected with NS (0.1ml/10g) subcutaneously, the MPTP group was injected with MPTP (30mg/kg, dissolved in NS, 0.15ml/10g) subcutaneously, the CU-CPT22 group was injected intraperitoneally with CU-CPT22 (3mg/kg, dissolved in DMSO, 40μl/10g; Selleck, S8677) [17] and in the CUCPT22+MPTP group, 30 minutes after intraperitoneal injection of CU-CPT22 (3mg/kg, dissolved in DMSO, 40μl/10g), MPTP (30mg/kg, dissolved in NS, 0.15ml /10g) was injected subcutaneously. ..

Saline:

Image Search Results

Schematic representation of the NP formulations. The PLGA NPs (left) consist of a PLGA matrix with embedded PEGylated phospholipids, some functionalized with a maleimide moiety for conjugation with targeting cyclic RGD peptides. The system also incorporates the therapeutic agent CU-CPT22, fluorescent probes (carboxyfluorescein or cyanine 5), and the MRI contrast agent Gd-DOTAMA. The liposome formulation (right) features a lipid bilayer formed by POPC and PEGylated phospholipids, also functionalized with maleimide moieties for cyclic RGD conjugation. Cholesterol is included to modulate membrane stability. Doxorubicin is encapsulated as the therapeutic agent, while fluorescent probes and the MRI contrast agent Prohance are integrated for imaging purposes.

Journal: International Journal of Nanomedicine

Article Title: Dual-Action Theranostic Nanoparticles Delivering Toll-Like Receptor 2 Inhibitors and Chemotherapy Target Breast Cancer Cells and the Tumor Microenvironment

doi: 10.2147/IJN.S556284

Figure Lengend Snippet: Schematic representation of the NP formulations. The PLGA NPs (left) consist of a PLGA matrix with embedded PEGylated phospholipids, some functionalized with a maleimide moiety for conjugation with targeting cyclic RGD peptides. The system also incorporates the therapeutic agent CU-CPT22, fluorescent probes (carboxyfluorescein or cyanine 5), and the MRI contrast agent Gd-DOTAMA. The liposome formulation (right) features a lipid bilayer formed by POPC and PEGylated phospholipids, also functionalized with maleimide moieties for cyclic RGD conjugation. Cholesterol is included to modulate membrane stability. Doxorubicin is encapsulated as the therapeutic agent, while fluorescent probes and the MRI contrast agent Prohance are integrated for imaging purposes.

Article Snippet: 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[maleimide(polyethyleneglycol)-2000] (ammonium salt) (DSPE-PEG2000-maleimide), 1,2-distearoyl-sn-glycero-3-phosphoethanolamine-N-[methoxy(polyethylene gly-col)-2000] (ammonium salt) (DPPE-PEG2000-methoxy), (1,2-dioleoyl-sn-glycero-3-poshosphoethanolamine-N-(carboxyfluorescein) (ammonium salt) (DOPE-CF) and 2-Oleoyl-1-palmitoyl-sn-glycero-3-phosphocholine (POPC) were purchased from Avanti Polar Lipids Inc. CU-CPT22 was purchased from Tocris Bioscience.

Techniques: Conjugation Assay, Formulation, Membrane, Imaging

PLGA-CU inhibits TLR2 signaling. ( A ) Representative FACS histogram of the expression of TLR2 and α v β 3 integrin on 4T1 and WT-874 cells. Light grey histograms show the background signal obtained by staining cells with an isotype control antibody; dark grey histograms show the signal obtained by staining with the specific monoclonal antibodies. ( B ) FACS analysis of PLGA-CU internalization into 4T1 and WT-874 cells incubated for 4 h at 37° C with 5 µM FITC-containing PLGA-CU or untargeted PLGA-CU, ie PLGA-CU not decorated with RGD. The graphs report the individual values and means ± SEM of the FITC MFI measured from two independent experiments. Representative FACS histograms are shown. ( C ) FACS analysis of PLGA-CU internalization into 4T1 and WT-874 cells incubated for 1 h at 37° C or 4° C with 5 µM FITC-containing PLGA-CU. An aliquot of cells was subjected to acidic stripping to remove membrane-bound PLGA-CU before analysis. The graphs report the individual values and means ± SEM of the FITC MFI measured from two independent experiments. Representative FACS histograms are shown. ( D ) FACS analysis of p65 NF-κB phosphorylation in WT-874 cells treated with PGN-SA (200 µg/mL) ± 5 µM CU-CPT22 or PLGA-CU for 24 h or left untreated. The individual values and means ± SEM of mean fluorescence intensity (MFI) from three independent experiments are reported, as well as representative FACS histograms where light grey histograms show the signal obtained with an isotype control antibody, dark grey histograms with the specific monoclonal antibody. **P < 0.01; ***P < 0.001, ****P < 0.0001, One-Way ANOVA.

Journal: International Journal of Nanomedicine

Article Title: Dual-Action Theranostic Nanoparticles Delivering Toll-Like Receptor 2 Inhibitors and Chemotherapy Target Breast Cancer Cells and the Tumor Microenvironment

doi: 10.2147/IJN.S556284

Figure Lengend Snippet: PLGA-CU inhibits TLR2 signaling. ( A ) Representative FACS histogram of the expression of TLR2 and α v β 3 integrin on 4T1 and WT-874 cells. Light grey histograms show the background signal obtained by staining cells with an isotype control antibody; dark grey histograms show the signal obtained by staining with the specific monoclonal antibodies. ( B ) FACS analysis of PLGA-CU internalization into 4T1 and WT-874 cells incubated for 4 h at 37° C with 5 µM FITC-containing PLGA-CU or untargeted PLGA-CU, ie PLGA-CU not decorated with RGD. The graphs report the individual values and means ± SEM of the FITC MFI measured from two independent experiments. Representative FACS histograms are shown. ( C ) FACS analysis of PLGA-CU internalization into 4T1 and WT-874 cells incubated for 1 h at 37° C or 4° C with 5 µM FITC-containing PLGA-CU. An aliquot of cells was subjected to acidic stripping to remove membrane-bound PLGA-CU before analysis. The graphs report the individual values and means ± SEM of the FITC MFI measured from two independent experiments. Representative FACS histograms are shown. ( D ) FACS analysis of p65 NF-κB phosphorylation in WT-874 cells treated with PGN-SA (200 µg/mL) ± 5 µM CU-CPT22 or PLGA-CU for 24 h or left untreated. The individual values and means ± SEM of mean fluorescence intensity (MFI) from three independent experiments are reported, as well as representative FACS histograms where light grey histograms show the signal obtained with an isotype control antibody, dark grey histograms with the specific monoclonal antibody. **P < 0.01; ***P < 0.001, ****P < 0.0001, One-Way ANOVA.

Techniques: Expressing, Staining, Control, Bioprocessing, Incubation, Stripping Membranes, Membrane, Phospho-proteomics, Fluorescence

PLGA-CU and LIPO-DOXO impair breast cancer cell viability. MTT assays on 4T1 and WT-874 cell lines treated for 48 h with ( A ) empty PLGA, PLGA-CU or free CU-CPT22 or ( C ) empty liposome, LIPO-DOXO or free doxorubicin at various concentrations. Cell viability of the same cell lines treated with ( B ) 5 μM PLGA-CU or CU-CPT22 for 48 h with or with ( D ) 1 μM LIPO-DOXO or doxorubicin, or with empty NPs (N = 3 independent experiments). ( E – G ) 4T1, WT-879, and MDA-MB-231 cells were treated with PLGA-CU, LIPO-DOXO or the free drugs for 48 h and analyzed using Annexin-V/propidium iodide FACS staining. Representative density plots are shown. The graphs show individual values and means ± SEM of the % of Annexin-V + from 6 independent experiments. *P < 0.05, **P < 0.01; ***P < 0.001, ****P < 0.0001, One-Way ANOVA.

Journal: International Journal of Nanomedicine

Article Title: Dual-Action Theranostic Nanoparticles Delivering Toll-Like Receptor 2 Inhibitors and Chemotherapy Target Breast Cancer Cells and the Tumor Microenvironment

doi: 10.2147/IJN.S556284

Figure Lengend Snippet: PLGA-CU and LIPO-DOXO impair breast cancer cell viability. MTT assays on 4T1 and WT-874 cell lines treated for 48 h with ( A ) empty PLGA, PLGA-CU or free CU-CPT22 or ( C ) empty liposome, LIPO-DOXO or free doxorubicin at various concentrations. Cell viability of the same cell lines treated with ( B ) 5 μM PLGA-CU or CU-CPT22 for 48 h with or with ( D ) 1 μM LIPO-DOXO or doxorubicin, or with empty NPs (N = 3 independent experiments). ( E – G ) 4T1, WT-879, and MDA-MB-231 cells were treated with PLGA-CU, LIPO-DOXO or the free drugs for 48 h and analyzed using Annexin-V/propidium iodide FACS staining. Representative density plots are shown. The graphs show individual values and means ± SEM of the % of Annexin-V + from 6 independent experiments. *P < 0.05, **P < 0.01; ***P < 0.001, ****P < 0.0001, One-Way ANOVA.

Techniques: Staining

PLGA-CU prevents doxorubicin-induced NF-kB activation. ( A ) FACS analysis of p65 NF-κB phosphorylation in WT-874 cells treated with 5 µM CU-CPT22 or PLGA-CU and/or 1 µM LIPO-DOXO or doxorubicin for 48 h, or left untreated. The individual values and means ± SEM of mean fluorescence intensity (MFI) from three independent experiments are reported, as well as representative FACS histograms where light grey histograms show the signal obtained with an isotype control antibody, dark grey histograms with the specific monoclonal antibody. ( B and C ) Representative Western blot analysis of phosphorylated and total p65 NF-κB in 4T1 and MDA-MB-231 cells treated as in ( A ). The graphs report the individual values and means ± SEM of the fold increase in NF-κB phosphorylation in treated samples as compared to control cells cultured in medium from three independent experiments. The black dotted line indicates the baseline activation level of control (medium) cells. ( D and E ) ELISA of IL-6 and TGF-β released into the supernatant of 4T1 cells cultured for 48 h as described in ( A ). ( F and G ) Representative images of tumorspheres (Magnification 10X), and graph showing sphere-generating ability (number of tumorspheres generated every 10 3 plated cells) of 4T1 cells cultured for 5 days in tumorsphere-forming conditions in the absence or presence of IL-6 (10 ng/mL) or PGN-SA (200 µg/mL). ( H ) Means ± SEM of the percentage of Sca1 + cells in 4T1 tumorspheres treated as in ( F ). ( I ) MTT assays on 4T1 cells treated for 48 h with IL-6 (10 ng/mL) or PGN-SA (200 µg/mL). The black dotted line represents the viability of the control condition, normalized to 100%. Deviations above or below this line indicate an increase or decrease in cell viability relative to the control. In all panels, N = 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, One-way ANOVA.

Journal: International Journal of Nanomedicine

Article Title: Dual-Action Theranostic Nanoparticles Delivering Toll-Like Receptor 2 Inhibitors and Chemotherapy Target Breast Cancer Cells and the Tumor Microenvironment

doi: 10.2147/IJN.S556284

Figure Lengend Snippet: PLGA-CU prevents doxorubicin-induced NF-kB activation. ( A ) FACS analysis of p65 NF-κB phosphorylation in WT-874 cells treated with 5 µM CU-CPT22 or PLGA-CU and/or 1 µM LIPO-DOXO or doxorubicin for 48 h, or left untreated. The individual values and means ± SEM of mean fluorescence intensity (MFI) from three independent experiments are reported, as well as representative FACS histograms where light grey histograms show the signal obtained with an isotype control antibody, dark grey histograms with the specific monoclonal antibody. ( B and C ) Representative Western blot analysis of phosphorylated and total p65 NF-κB in 4T1 and MDA-MB-231 cells treated as in ( A ). The graphs report the individual values and means ± SEM of the fold increase in NF-κB phosphorylation in treated samples as compared to control cells cultured in medium from three independent experiments. The black dotted line indicates the baseline activation level of control (medium) cells. ( D and E ) ELISA of IL-6 and TGF-β released into the supernatant of 4T1 cells cultured for 48 h as described in ( A ). ( F and G ) Representative images of tumorspheres (Magnification 10X), and graph showing sphere-generating ability (number of tumorspheres generated every 10 3 plated cells) of 4T1 cells cultured for 5 days in tumorsphere-forming conditions in the absence or presence of IL-6 (10 ng/mL) or PGN-SA (200 µg/mL). ( H ) Means ± SEM of the percentage of Sca1 + cells in 4T1 tumorspheres treated as in ( F ). ( I ) MTT assays on 4T1 cells treated for 48 h with IL-6 (10 ng/mL) or PGN-SA (200 µg/mL). The black dotted line represents the viability of the control condition, normalized to 100%. Deviations above or below this line indicate an increase or decrease in cell viability relative to the control. In all panels, N = 3 independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, One-way ANOVA.

Techniques: Activation Assay, Phospho-proteomics, Fluorescence, Control, Western Blot, Cell Culture, Enzyme-linked Immunosorbent Assay, Generated

PLGA-CU impairs angiogenesis. ( A ) Individual values and means ± SEM of the % of CD31 + cells and ( B ) representative CD31 IHC staining of tumors. Magnification X20. ( C – E ) ELISA analysis of VEGF released into the supernatant by 4T1, MDA-MB-231 or Bend.3 cells treated with PLGA-CU and/or LIPO-DOXO or free CU-CPT22 or doxorubicin for 48 h or left untreated. The graphs show individual values and means ± SEM of VEGF concentration from three independent experiments. ( F ) bEnd.3 cells were treated as in E, then apoptosis was analyzed. The graph shows individual values and means ± SEM of the % of Annexin-V + from three independent experiments. *P < 0.05, **P < 0.01; ***P < 0.001, ****P < 0.0001, Two-Way ( A ) or One-Way ANOVA.

Journal: International Journal of Nanomedicine

Article Title: Dual-Action Theranostic Nanoparticles Delivering Toll-Like Receptor 2 Inhibitors and Chemotherapy Target Breast Cancer Cells and the Tumor Microenvironment

doi: 10.2147/IJN.S556284

Figure Lengend Snippet: PLGA-CU impairs angiogenesis. ( A ) Individual values and means ± SEM of the % of CD31 + cells and ( B ) representative CD31 IHC staining of tumors. Magnification X20. ( C – E ) ELISA analysis of VEGF released into the supernatant by 4T1, MDA-MB-231 or Bend.3 cells treated with PLGA-CU and/or LIPO-DOXO or free CU-CPT22 or doxorubicin for 48 h or left untreated. The graphs show individual values and means ± SEM of VEGF concentration from three independent experiments. ( F ) bEnd.3 cells were treated as in E, then apoptosis was analyzed. The graph shows individual values and means ± SEM of the % of Annexin-V + from three independent experiments. *P < 0.05, **P < 0.01; ***P < 0.001, ****P < 0.0001, Two-Way ( A ) or One-Way ANOVA.

Techniques: Immunohistochemistry, Enzyme-linked Immunosorbent Assay, Concentration Assay

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tlr2 inhibition (Selleck Chemicals)

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Control:

Incubation:

Expressing:

Quantitative RT-PCR:

In Vivo:

Inhibition:

Injection:

Saline:

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