cu cpt22 Search Results


cu cpt22  (MedChemExpress)
94
MedChemExpress cu cpt22
ZnONPs induced cytotoxicity and innate immune responses through Toll-like receptor (TLR) signaling in THP-1-derived macrophages. THP-1 cells were incubated for 24 h in the presence of 10 ng/ml PMA and then exposed to various concentrations of ZnONPs for different times. A Effects of ZnONPs on THP-1-derived macrophage viability after 24 or 48 h. Cell viability was measured by MTT assays. B ZnONP-induced ROS generation in THP-1-derived macrophages. After being exposed to ZnONPs, the cells were incubated with 10 μM DCFH-DA for 30 min to stain H 2 O 2 and analyzed by flow cytometry. Histograms show the percentages of DCFH-DA fluorescence compared with the control. The data are presented as the mean ± SD from three independent experiments. (* p < 0.05, compared with control) C THP-1-derived macrophages were treated with ZnONPs (10 and 15 μg/ml) for 18 h, and the mRNA expression of TLR1, TLR3 and TLR6 was examined by RT‒qPCR and normalized to GAPDH expression. The data were presented as the mean ± SD from three independent experiments. The results showed that ZnONPs significantly triggered TLR1 and TLR3 activation. D THP-1-derived macrophages were treated with ZnONPs (10 μg/ml) for various times, and NFκB (p-p65) protein expression was analyzed by western blotting. E The mRNA levels of the proinflammatory cytokines TNF-α and IL-1β were determined by RT‒qPCR and normalized to GAPDH expression. The data are presented as the mean ± SD from three independent experiments. ZnONPs increased TNF-α and IL-1β mRNA expression at 18 h. (* p < 0.05, ** p < 0.01 compared with control). F THP-1-derived macrophages were treated with ZnONPs (10 μg/ml), and <t>CU-CPT22</t> or CU-CPT 4a for 16 h, then NFκB (p-p65) protein expression was analyzed by western blotting. CU-CPT22 and CU-CPT 4a are inhibitors specific to TLR1/2 and TLR3, respectively. G Cells were treated with ZnONPs (10 μg/ml), and CU-CPT22 (50 μM) or CU-CPT 4a (30 μM) for 24 h. TNF-α and IL-1β protein levels in the culture medium were measured by ELISA. The data were presented as the mean ± SD from three independent experiments. (* p < 0.05, ** p < 0.01 compared with control, # p < 0.05, ## p < 0.01 compared with ZnONPs alone)
Cu Cpt22, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 94 stars, based on 1 article reviews
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cu cpt22  (TargetMol)
93
TargetMol cu cpt22
ZnONPs induced cytotoxicity and innate immune responses through Toll-like receptor (TLR) signaling in THP-1-derived macrophages. THP-1 cells were incubated for 24 h in the presence of 10 ng/ml PMA and then exposed to various concentrations of ZnONPs for different times. A Effects of ZnONPs on THP-1-derived macrophage viability after 24 or 48 h. Cell viability was measured by MTT assays. B ZnONP-induced ROS generation in THP-1-derived macrophages. After being exposed to ZnONPs, the cells were incubated with 10 μM DCFH-DA for 30 min to stain H 2 O 2 and analyzed by flow cytometry. Histograms show the percentages of DCFH-DA fluorescence compared with the control. The data are presented as the mean ± SD from three independent experiments. (* p < 0.05, compared with control) C THP-1-derived macrophages were treated with ZnONPs (10 and 15 μg/ml) for 18 h, and the mRNA expression of TLR1, TLR3 and TLR6 was examined by RT‒qPCR and normalized to GAPDH expression. The data were presented as the mean ± SD from three independent experiments. The results showed that ZnONPs significantly triggered TLR1 and TLR3 activation. D THP-1-derived macrophages were treated with ZnONPs (10 μg/ml) for various times, and NFκB (p-p65) protein expression was analyzed by western blotting. E The mRNA levels of the proinflammatory cytokines TNF-α and IL-1β were determined by RT‒qPCR and normalized to GAPDH expression. The data are presented as the mean ± SD from three independent experiments. ZnONPs increased TNF-α and IL-1β mRNA expression at 18 h. (* p < 0.05, ** p < 0.01 compared with control). F THP-1-derived macrophages were treated with ZnONPs (10 μg/ml), and <t>CU-CPT22</t> or CU-CPT 4a for 16 h, then NFκB (p-p65) protein expression was analyzed by western blotting. CU-CPT22 and CU-CPT 4a are inhibitors specific to TLR1/2 and TLR3, respectively. G Cells were treated with ZnONPs (10 μg/ml), and CU-CPT22 (50 μM) or CU-CPT 4a (30 μM) for 24 h. TNF-α and IL-1β protein levels in the culture medium were measured by ELISA. The data were presented as the mean ± SD from three independent experiments. (* p < 0.05, ** p < 0.01 compared with control, # p < 0.05, ## p < 0.01 compared with ZnONPs alone)
Cu Cpt22, supplied by TargetMol, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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s8677  (Selleck Chemicals)
93
Selleck Chemicals s8677
ZnONPs induced cytotoxicity and innate immune responses through Toll-like receptor (TLR) signaling in THP-1-derived macrophages. THP-1 cells were incubated for 24 h in the presence of 10 ng/ml PMA and then exposed to various concentrations of ZnONPs for different times. A Effects of ZnONPs on THP-1-derived macrophage viability after 24 or 48 h. Cell viability was measured by MTT assays. B ZnONP-induced ROS generation in THP-1-derived macrophages. After being exposed to ZnONPs, the cells were incubated with 10 μM DCFH-DA for 30 min to stain H 2 O 2 and analyzed by flow cytometry. Histograms show the percentages of DCFH-DA fluorescence compared with the control. The data are presented as the mean ± SD from three independent experiments. (* p < 0.05, compared with control) C THP-1-derived macrophages were treated with ZnONPs (10 and 15 μg/ml) for 18 h, and the mRNA expression of TLR1, TLR3 and TLR6 was examined by RT‒qPCR and normalized to GAPDH expression. The data were presented as the mean ± SD from three independent experiments. The results showed that ZnONPs significantly triggered TLR1 and TLR3 activation. D THP-1-derived macrophages were treated with ZnONPs (10 μg/ml) for various times, and NFκB (p-p65) protein expression was analyzed by western blotting. E The mRNA levels of the proinflammatory cytokines TNF-α and IL-1β were determined by RT‒qPCR and normalized to GAPDH expression. The data are presented as the mean ± SD from three independent experiments. ZnONPs increased TNF-α and IL-1β mRNA expression at 18 h. (* p < 0.05, ** p < 0.01 compared with control). F THP-1-derived macrophages were treated with ZnONPs (10 μg/ml), and <t>CU-CPT22</t> or CU-CPT 4a for 16 h, then NFκB (p-p65) protein expression was analyzed by western blotting. CU-CPT22 and CU-CPT 4a are inhibitors specific to TLR1/2 and TLR3, respectively. G Cells were treated with ZnONPs (10 μg/ml), and CU-CPT22 (50 μM) or CU-CPT 4a (30 μM) for 24 h. TNF-α and IL-1β protein levels in the culture medium were measured by ELISA. The data were presented as the mean ± SD from three independent experiments. (* p < 0.05, ** p < 0.01 compared with control, # p < 0.05, ## p < 0.01 compared with ZnONPs alone)
S8677, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cucpt  (Tocris)
94
Tocris cucpt
ZnONPs induced cytotoxicity and innate immune responses through Toll-like receptor (TLR) signaling in THP-1-derived macrophages. THP-1 cells were incubated for 24 h in the presence of 10 ng/ml PMA and then exposed to various concentrations of ZnONPs for different times. A Effects of ZnONPs on THP-1-derived macrophage viability after 24 or 48 h. Cell viability was measured by MTT assays. B ZnONP-induced ROS generation in THP-1-derived macrophages. After being exposed to ZnONPs, the cells were incubated with 10 μM DCFH-DA for 30 min to stain H 2 O 2 and analyzed by flow cytometry. Histograms show the percentages of DCFH-DA fluorescence compared with the control. The data are presented as the mean ± SD from three independent experiments. (* p < 0.05, compared with control) C THP-1-derived macrophages were treated with ZnONPs (10 and 15 μg/ml) for 18 h, and the mRNA expression of TLR1, TLR3 and TLR6 was examined by RT‒qPCR and normalized to GAPDH expression. The data were presented as the mean ± SD from three independent experiments. The results showed that ZnONPs significantly triggered TLR1 and TLR3 activation. D THP-1-derived macrophages were treated with ZnONPs (10 μg/ml) for various times, and NFκB (p-p65) protein expression was analyzed by western blotting. E The mRNA levels of the proinflammatory cytokines TNF-α and IL-1β were determined by RT‒qPCR and normalized to GAPDH expression. The data are presented as the mean ± SD from three independent experiments. ZnONPs increased TNF-α and IL-1β mRNA expression at 18 h. (* p < 0.05, ** p < 0.01 compared with control). F THP-1-derived macrophages were treated with ZnONPs (10 μg/ml), and <t>CU-CPT22</t> or CU-CPT 4a for 16 h, then NFκB (p-p65) protein expression was analyzed by western blotting. CU-CPT22 and CU-CPT 4a are inhibitors specific to TLR1/2 and TLR3, respectively. G Cells were treated with ZnONPs (10 μg/ml), and CU-CPT22 (50 μM) or CU-CPT 4a (30 μM) for 24 h. TNF-α and IL-1β protein levels in the culture medium were measured by ELISA. The data were presented as the mean ± SD from three independent experiments. (* p < 0.05, ** p < 0.01 compared with control, # p < 0.05, ## p < 0.01 compared with ZnONPs alone)
Cucpt, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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tlr2 inhibitor cu cpt 22  (Tocris)
94
Tocris tlr2 inhibitor cu cpt 22
ZnONPs induced cytotoxicity and innate immune responses through Toll-like receptor (TLR) signaling in THP-1-derived macrophages. THP-1 cells were incubated for 24 h in the presence of 10 ng/ml PMA and then exposed to various concentrations of ZnONPs for different times. A Effects of ZnONPs on THP-1-derived macrophage viability after 24 or 48 h. Cell viability was measured by MTT assays. B ZnONP-induced ROS generation in THP-1-derived macrophages. After being exposed to ZnONPs, the cells were incubated with 10 μM DCFH-DA for 30 min to stain H 2 O 2 and analyzed by flow cytometry. Histograms show the percentages of DCFH-DA fluorescence compared with the control. The data are presented as the mean ± SD from three independent experiments. (* p < 0.05, compared with control) C THP-1-derived macrophages were treated with ZnONPs (10 and 15 μg/ml) for 18 h, and the mRNA expression of TLR1, TLR3 and TLR6 was examined by RT‒qPCR and normalized to GAPDH expression. The data were presented as the mean ± SD from three independent experiments. The results showed that ZnONPs significantly triggered TLR1 and TLR3 activation. D THP-1-derived macrophages were treated with ZnONPs (10 μg/ml) for various times, and NFκB (p-p65) protein expression was analyzed by western blotting. E The mRNA levels of the proinflammatory cytokines TNF-α and IL-1β were determined by RT‒qPCR and normalized to GAPDH expression. The data are presented as the mean ± SD from three independent experiments. ZnONPs increased TNF-α and IL-1β mRNA expression at 18 h. (* p < 0.05, ** p < 0.01 compared with control). F THP-1-derived macrophages were treated with ZnONPs (10 μg/ml), and <t>CU-CPT22</t> or CU-CPT 4a for 16 h, then NFκB (p-p65) protein expression was analyzed by western blotting. CU-CPT22 and CU-CPT 4a are inhibitors specific to TLR1/2 and TLR3, respectively. G Cells were treated with ZnONPs (10 μg/ml), and CU-CPT22 (50 μM) or CU-CPT 4a (30 μM) for 24 h. TNF-α and IL-1β protein levels in the culture medium were measured by ELISA. The data were presented as the mean ± SD from three independent experiments. (* p < 0.05, ** p < 0.01 compared with control, # p < 0.05, ## p < 0.01 compared with ZnONPs alone)
Tlr2 Inhibitor Cu Cpt 22, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cu-ctp22 tlr1/tlr2 antagonist  (Merck KGaA)
90
Merck KGaA cu-ctp22 tlr1/tlr2 antagonist
ZnONPs induced cytotoxicity and innate immune responses through Toll-like receptor (TLR) signaling in THP-1-derived macrophages. THP-1 cells were incubated for 24 h in the presence of 10 ng/ml PMA and then exposed to various concentrations of ZnONPs for different times. A Effects of ZnONPs on THP-1-derived macrophage viability after 24 or 48 h. Cell viability was measured by MTT assays. B ZnONP-induced ROS generation in THP-1-derived macrophages. After being exposed to ZnONPs, the cells were incubated with 10 μM DCFH-DA for 30 min to stain H 2 O 2 and analyzed by flow cytometry. Histograms show the percentages of DCFH-DA fluorescence compared with the control. The data are presented as the mean ± SD from three independent experiments. (* p < 0.05, compared with control) C THP-1-derived macrophages were treated with ZnONPs (10 and 15 μg/ml) for 18 h, and the mRNA expression of TLR1, TLR3 and TLR6 was examined by RT‒qPCR and normalized to GAPDH expression. The data were presented as the mean ± SD from three independent experiments. The results showed that ZnONPs significantly triggered TLR1 and TLR3 activation. D THP-1-derived macrophages were treated with ZnONPs (10 μg/ml) for various times, and NFκB (p-p65) protein expression was analyzed by western blotting. E The mRNA levels of the proinflammatory cytokines TNF-α and IL-1β were determined by RT‒qPCR and normalized to GAPDH expression. The data are presented as the mean ± SD from three independent experiments. ZnONPs increased TNF-α and IL-1β mRNA expression at 18 h. (* p < 0.05, ** p < 0.01 compared with control). F THP-1-derived macrophages were treated with ZnONPs (10 μg/ml), and <t>CU-CPT22</t> or CU-CPT 4a for 16 h, then NFκB (p-p65) protein expression was analyzed by western blotting. CU-CPT22 and CU-CPT 4a are inhibitors specific to TLR1/2 and TLR3, respectively. G Cells were treated with ZnONPs (10 μg/ml), and CU-CPT22 (50 μM) or CU-CPT 4a (30 μM) for 24 h. TNF-α and IL-1β protein levels in the culture medium were measured by ELISA. The data were presented as the mean ± SD from three independent experiments. (* p < 0.05, ** p < 0.01 compared with control, # p < 0.05, ## p < 0.01 compared with ZnONPs alone)
Cu Ctp22 Tlr1/Tlr2 Antagonist, 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
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cu-cpt22  (Cayman Chemical)
90
Cayman Chemical cu-cpt22
Age-dependent expressions of Pg-LPS receptors, <t>TLR2,</t> and TLR4, on the surface of CD11b+CSF1r-eGFP+ OCPs. Osteoclast precursors (OCPs) were FACS sorted from the spleen of young (2 months old) and aged (24 months old) CSF1r-eGFP-KI mice and then were stimulated with macrophage colony-stimulating factor (M-CSF) (30 ng/ml) and RANKL (5 ng/ml). After 24 h of stimulation, the expression of TLR2 (a and b) and TLR4 (c and d) was evaluated by multicolor flow cytometry. ***p < 0.001
Cu Cpt22, supplied by Cayman Chemical, 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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cu-cpt22 solution  (Fisher Scientific)
90
Fisher Scientific cu-cpt22 solution
Age-dependent expressions of Pg-LPS receptors, <t>TLR2,</t> and TLR4, on the surface of CD11b+CSF1r-eGFP+ OCPs. Osteoclast precursors (OCPs) were FACS sorted from the spleen of young (2 months old) and aged (24 months old) CSF1r-eGFP-KI mice and then were stimulated with macrophage colony-stimulating factor (M-CSF) (30 ng/ml) and RANKL (5 ng/ml). After 24 h of stimulation, the expression of TLR2 (a and b) and TLR4 (c and d) was evaluated by multicolor flow cytometry. ***p < 0.001
Cu Cpt22 Solution, supplied by Fisher Scientific, 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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cu cpt 22  (GlpBio Technology Inc)
90
GlpBio Technology Inc cu cpt 22
Age-dependent expressions of Pg-LPS receptors, <t>TLR2,</t> and TLR4, on the surface of CD11b+CSF1r-eGFP+ OCPs. Osteoclast precursors (OCPs) were FACS sorted from the spleen of young (2 months old) and aged (24 months old) CSF1r-eGFP-KI mice and then were stimulated with macrophage colony-stimulating factor (M-CSF) (30 ng/ml) and RANKL (5 ng/ml). After 24 h of stimulation, the expression of TLR2 (a and b) and TLR4 (c and d) was evaluated by multicolor flow cytometry. ***p < 0.001
Cu Cpt 22, supplied by GlpBio Technology Inc, 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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cu cpt 22  (Cayman Chemical)
N/A
CU CPT 22
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cu cpt 22  (Aladdin Scientific Corporation)
N/A
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cu cpt 22  (BOC Sciences)
N/A
CU CPT 22 is a selective TLR1/2 inhibitor (IC50 = 0.58 μM).
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ZnONPs induced cytotoxicity and innate immune responses through Toll-like receptor (TLR) signaling in THP-1-derived macrophages. THP-1 cells were incubated for 24 h in the presence of 10 ng/ml PMA and then exposed to various concentrations of ZnONPs for different times. A Effects of ZnONPs on THP-1-derived macrophage viability after 24 or 48 h. Cell viability was measured by MTT assays. B ZnONP-induced ROS generation in THP-1-derived macrophages. After being exposed to ZnONPs, the cells were incubated with 10 μM DCFH-DA for 30 min to stain H 2 O 2 and analyzed by flow cytometry. Histograms show the percentages of DCFH-DA fluorescence compared with the control. The data are presented as the mean ± SD from three independent experiments. (* p < 0.05, compared with control) C THP-1-derived macrophages were treated with ZnONPs (10 and 15 μg/ml) for 18 h, and the mRNA expression of TLR1, TLR3 and TLR6 was examined by RT‒qPCR and normalized to GAPDH expression. The data were presented as the mean ± SD from three independent experiments. The results showed that ZnONPs significantly triggered TLR1 and TLR3 activation. D THP-1-derived macrophages were treated with ZnONPs (10 μg/ml) for various times, and NFκB (p-p65) protein expression was analyzed by western blotting. E The mRNA levels of the proinflammatory cytokines TNF-α and IL-1β were determined by RT‒qPCR and normalized to GAPDH expression. The data are presented as the mean ± SD from three independent experiments. ZnONPs increased TNF-α and IL-1β mRNA expression at 18 h. (* p < 0.05, ** p < 0.01 compared with control). F THP-1-derived macrophages were treated with ZnONPs (10 μg/ml), and CU-CPT22 or CU-CPT 4a for 16 h, then NFκB (p-p65) protein expression was analyzed by western blotting. CU-CPT22 and CU-CPT 4a are inhibitors specific to TLR1/2 and TLR3, respectively. G Cells were treated with ZnONPs (10 μg/ml), and CU-CPT22 (50 μM) or CU-CPT 4a (30 μM) for 24 h. TNF-α and IL-1β protein levels in the culture medium were measured by ELISA. The data were presented as the mean ± SD from three independent experiments. (* p < 0.05, ** p < 0.01 compared with control, # p < 0.05, ## p < 0.01 compared with ZnONPs alone)

Journal: Particle and Fibre Toxicology

Article Title: Zinc oxide nanoparticles exacerbate skin epithelial cell damage by upregulating pro-inflammatory cytokines and exosome secretion in M1 macrophages following UVB irradiation-induced skin injury

doi: 10.1186/s12989-024-00571-z

Figure Lengend Snippet: ZnONPs induced cytotoxicity and innate immune responses through Toll-like receptor (TLR) signaling in THP-1-derived macrophages. THP-1 cells were incubated for 24 h in the presence of 10 ng/ml PMA and then exposed to various concentrations of ZnONPs for different times. A Effects of ZnONPs on THP-1-derived macrophage viability after 24 or 48 h. Cell viability was measured by MTT assays. B ZnONP-induced ROS generation in THP-1-derived macrophages. After being exposed to ZnONPs, the cells were incubated with 10 μM DCFH-DA for 30 min to stain H 2 O 2 and analyzed by flow cytometry. Histograms show the percentages of DCFH-DA fluorescence compared with the control. The data are presented as the mean ± SD from three independent experiments. (* p < 0.05, compared with control) C THP-1-derived macrophages were treated with ZnONPs (10 and 15 μg/ml) for 18 h, and the mRNA expression of TLR1, TLR3 and TLR6 was examined by RT‒qPCR and normalized to GAPDH expression. The data were presented as the mean ± SD from three independent experiments. The results showed that ZnONPs significantly triggered TLR1 and TLR3 activation. D THP-1-derived macrophages were treated with ZnONPs (10 μg/ml) for various times, and NFκB (p-p65) protein expression was analyzed by western blotting. E The mRNA levels of the proinflammatory cytokines TNF-α and IL-1β were determined by RT‒qPCR and normalized to GAPDH expression. The data are presented as the mean ± SD from three independent experiments. ZnONPs increased TNF-α and IL-1β mRNA expression at 18 h. (* p < 0.05, ** p < 0.01 compared with control). F THP-1-derived macrophages were treated with ZnONPs (10 μg/ml), and CU-CPT22 or CU-CPT 4a for 16 h, then NFκB (p-p65) protein expression was analyzed by western blotting. CU-CPT22 and CU-CPT 4a are inhibitors specific to TLR1/2 and TLR3, respectively. G Cells were treated with ZnONPs (10 μg/ml), and CU-CPT22 (50 μM) or CU-CPT 4a (30 μM) for 24 h. TNF-α and IL-1β protein levels in the culture medium were measured by ELISA. The data were presented as the mean ± SD from three independent experiments. (* p < 0.05, ** p < 0.01 compared with control, # p < 0.05, ## p < 0.01 compared with ZnONPs alone)

Article Snippet: CU-CPT22 and CU-CPT4a were purchased from MedChemExpress (NJ, USA).

Techniques: Derivative Assay, Incubation, Staining, Flow Cytometry, Fluorescence, Control, Expressing, Activation Assay, Western Blot, Enzyme-linked Immunosorbent Assay

Age-dependent expressions of Pg-LPS receptors, TLR2, and TLR4, on the surface of CD11b+CSF1r-eGFP+ OCPs. Osteoclast precursors (OCPs) were FACS sorted from the spleen of young (2 months old) and aged (24 months old) CSF1r-eGFP-KI mice and then were stimulated with macrophage colony-stimulating factor (M-CSF) (30 ng/ml) and RANKL (5 ng/ml). After 24 h of stimulation, the expression of TLR2 (a and b) and TLR4 (c and d) was evaluated by multicolor flow cytometry. ***p < 0.001

Journal: GeroScience

Article Title: Contribution of Porphyromonas gingivalis lipopolysaccharide to experimental periodontitis in relation to aging

doi: 10.1007/s11357-020-00258-1

Figure Lengend Snippet: Age-dependent expressions of Pg-LPS receptors, TLR2, and TLR4, on the surface of CD11b+CSF1r-eGFP+ OCPs. Osteoclast precursors (OCPs) were FACS sorted from the spleen of young (2 months old) and aged (24 months old) CSF1r-eGFP-KI mice and then were stimulated with macrophage colony-stimulating factor (M-CSF) (30 ng/ml) and RANKL (5 ng/ml). After 24 h of stimulation, the expression of TLR2 (a and b) and TLR4 (c and d) was evaluated by multicolor flow cytometry. ***p < 0.001

Article Snippet: FACS-sorted CD11b+CSF1r-eGFP+ OCPs were seeded in 96-well plates at a density of 1 × 10 4 cells/well in α-MEM medium (Life Technologies) containing 10% FBS (Atlanta Biologicals) and 30 ng/ml of M-CSF and 5 ng/ml of RANKL (BioLegend) recombinant proteins in the presence or absence of various concentrations of ultrapure Pg -LPS (1, or 10 ng/ml; InvivoGen), CU-CPT22 (1 and 10 μM; TLR2 antagonist; Cayman Chemical), and TAK242 (1 and 10 μM; TLR4 antagonist; Cayman Chemical).

Techniques: Expressing, Flow Cytometry

The effects of Pg-LPS and TLR’s antagonists on RANKL-induced osteoclastogenesis in relation to aging. Microscopic evaluation (a) of the TRAP staining and quantification of the number of TRAP+ multinucleated cells (b) in the RANKL-stimulated young and aged OCPs exposed to Pg-LPS in vitro. Effects of TLR4 (CAS 243984-11-4) and TLR2 antagonists (CU-CPT22) on young (c) and aged (d) RANKL-stimulated OCPs exposed to Pg-LPS. OCPs were FACS sorted from the spleen of young and aged mice and then were stimulated with RANKL in the presence or absence of various concentrations of Pg-LPS as well as TLR2 and TLR4 antagonists. The cells were evaluated at day 6 after stimulation. **p < 0.01, ***p < 0.001

Journal: GeroScience

Article Title: Contribution of Porphyromonas gingivalis lipopolysaccharide to experimental periodontitis in relation to aging

doi: 10.1007/s11357-020-00258-1

Figure Lengend Snippet: The effects of Pg-LPS and TLR’s antagonists on RANKL-induced osteoclastogenesis in relation to aging. Microscopic evaluation (a) of the TRAP staining and quantification of the number of TRAP+ multinucleated cells (b) in the RANKL-stimulated young and aged OCPs exposed to Pg-LPS in vitro. Effects of TLR4 (CAS 243984-11-4) and TLR2 antagonists (CU-CPT22) on young (c) and aged (d) RANKL-stimulated OCPs exposed to Pg-LPS. OCPs were FACS sorted from the spleen of young and aged mice and then were stimulated with RANKL in the presence or absence of various concentrations of Pg-LPS as well as TLR2 and TLR4 antagonists. The cells were evaluated at day 6 after stimulation. **p < 0.01, ***p < 0.001

Article Snippet: FACS-sorted CD11b+CSF1r-eGFP+ OCPs were seeded in 96-well plates at a density of 1 × 10 4 cells/well in α-MEM medium (Life Technologies) containing 10% FBS (Atlanta Biologicals) and 30 ng/ml of M-CSF and 5 ng/ml of RANKL (BioLegend) recombinant proteins in the presence or absence of various concentrations of ultrapure Pg -LPS (1, or 10 ng/ml; InvivoGen), CU-CPT22 (1 and 10 μM; TLR2 antagonist; Cayman Chemical), and TAK242 (1 and 10 μM; TLR4 antagonist; Cayman Chemical).

Techniques: Staining, In Vitro