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mcc950 (MedChemExpress)

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AGEs activate the NLRP3 inflammasome in cardiomyocytes via the RAGE/ROS/NF‐ κ B signaling axis. (a–k) Primary neonatal mouse cardiomyocytes were pretreated with or without the RAGE <t>inhibitor</t> <t>FPS‐ZM1</t> (20 μ M) or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (a) Representative Western blots of phospho‐NF‐ κ B p65 (pp65), total NF‐ κ B p65, NLRP3, caspase‐1 P20, and N‐GSDMD. (b–e) Quantitative analysis of the protein levels of (b) pp65/NF‐ κ B p65, (c) NLRP3, (d) caspase‐1 P20, and (e) N‐GSDMD, n = 4. (f,g) Concentrations of (f) I L‐1 β and (g) IL‐18 in the cell culture supernatant were measured by ELISA, n = 4. (h,i) Intracellular ROS levels were detected using the DCFHDA fluorescent probe. (h) Representative fluorescence images. Scale bar, 50 μ m. (i) Quantitative analysis of ROS fluorescence intensity, n = 4. (j,k) ASC oligomerization was assessed by immunofluorescence. (j) Representative images showing ASC specks. Scale bar, 10 μ m. (k) Quantification of ASC fluorescence intensity, n = 4. (l–v) Cardiomyocytes were pretreated with or without the ROS scavenger NAC (10 μ M) or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (l) Representative immunoblots of the indicated proteins. (m–p) Quantitative analysis of (m) pp65/NF‐ κ B p65, (n) NLRP3, (o) caspase‐1 P20, and (p) N‐GSDMD, n = 4. (q,r) ELISA analysis of (q) IL‐1 β and (r) IL‐18 levels in the supernatant, n = 4. (s,t) Intracellular ROS levels were measured as above. (s) Representative images. Scale bar, 50 μ m. (T) Fluorescence quantification, n = 4. (u,v) Assessment of ASC speck formation. (u) Representative images. Scale bar, 10 μ m. (v) Quantification of ASC fluorescence intensity, n = 4.

Mcc950, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 658 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mcc950 - by Bioz Stars, 2026-11

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1) Product Images from "The AGEs/RAGE Axis Contributes to Myocardial Cell Death in Type 1 Diabetic Cardiomyopathy via the ROS/NF‐ κ B/NLRP3 Inflammasome Pathway"

Article Title: The AGEs/RAGE Axis Contributes to Myocardial Cell Death in Type 1 Diabetic Cardiomyopathy via the ROS/NF‐ κ B/NLRP3 Inflammasome Pathway

Journal: Journal of Diabetes Research

doi: 10.1155/jdr/6438008

Figure Legend Snippet: AGEs activate the NLRP3 inflammasome in cardiomyocytes via the RAGE/ROS/NF‐ κ B signaling axis. (a–k) Primary neonatal mouse cardiomyocytes were pretreated with or without the RAGE inhibitor FPS‐ZM1 (20 μ M) or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (a) Representative Western blots of phospho‐NF‐ κ B p65 (pp65), total NF‐ κ B p65, NLRP3, caspase‐1 P20, and N‐GSDMD. (b–e) Quantitative analysis of the protein levels of (b) pp65/NF‐ κ B p65, (c) NLRP3, (d) caspase‐1 P20, and (e) N‐GSDMD, n = 4. (f,g) Concentrations of (f) I L‐1 β and (g) IL‐18 in the cell culture supernatant were measured by ELISA, n = 4. (h,i) Intracellular ROS levels were detected using the DCFHDA fluorescent probe. (h) Representative fluorescence images. Scale bar, 50 μ m. (i) Quantitative analysis of ROS fluorescence intensity, n = 4. (j,k) ASC oligomerization was assessed by immunofluorescence. (j) Representative images showing ASC specks. Scale bar, 10 μ m. (k) Quantification of ASC fluorescence intensity, n = 4. (l–v) Cardiomyocytes were pretreated with or without the ROS scavenger NAC (10 μ M) or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (l) Representative immunoblots of the indicated proteins. (m–p) Quantitative analysis of (m) pp65/NF‐ κ B p65, (n) NLRP3, (o) caspase‐1 P20, and (p) N‐GSDMD, n = 4. (q,r) ELISA analysis of (q) IL‐1 β and (r) IL‐18 levels in the supernatant, n = 4. (s,t) Intracellular ROS levels were measured as above. (s) Representative images. Scale bar, 50 μ m. (T) Fluorescence quantification, n = 4. (u,v) Assessment of ASC speck formation. (u) Representative images. Scale bar, 10 μ m. (v) Quantification of ASC fluorescence intensity, n = 4.

Techniques Used: Western Blot, Analysis, Cell Culture, Enzyme-linked Immunosorbent Assay, Fluorescence, Immunofluorescence

AGEs induce pyroptotic cell death in cardiomyocytes through the RAGE/ROS/NLRP3 pathway. Primary neonatal mouse cardiomyocytes were pretreated with or without FPS‐ZM1 (20 μ M), NAC (10 μ M), MCC950 (10 μ M), or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (a) Representative fluorescence images of SYTOX green staining. Scale bar, 200 μ m. (b) Quantitative analysis of SYTOX‐positive cells, n = 4. (c) Representative fluorescence images of propidium iodide (PI) uptake. Scale bar, 100 μ m. (d) Quantitative analysis of PI‐positive cells, n = 4. (e) Lactate dehydrogenase (LDH) release in the cell culture supernatant was measured, n = 4.

Figure Legend Snippet: AGEs induce pyroptotic cell death in cardiomyocytes through the RAGE/ROS/NLRP3 pathway. Primary neonatal mouse cardiomyocytes were pretreated with or without FPS‐ZM1 (20 μ M), NAC (10 μ M), MCC950 (10 μ M), or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (a) Representative fluorescence images of SYTOX green staining. Scale bar, 200 μ m. (b) Quantitative analysis of SYTOX‐positive cells, n = 4. (c) Representative fluorescence images of propidium iodide (PI) uptake. Scale bar, 100 μ m. (d) Quantitative analysis of PI‐positive cells, n = 4. (e) Lactate dehydrogenase (LDH) release in the cell culture supernatant was measured, n = 4.

Techniques Used: Fluorescence, Staining, Analysis, Cell Culture

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Article Title: Bergapten Alleviates Periodontitis by Suppressing NLRP3 Inflammasome Activation via Mitophagy-Induced Disruption of NEK7-NLRP3 Interaction
Article Snippet: BeG (cat. no. HY-N0370), MHY1485 (cat. no. HY-B0795), MCC950 (cat. no. HY-12815), R837 (cat. no. HY-B0180A), chloroquine (cat. no. HY-17589A) and nigericin (cat. no. HY-127019) were purchased from MedChemExpress (Monmouth Junction, NJ, USA).

Article Title: Targeting the Keap1/Nrf2 pathway: Ginkgolide B mitigates oxidative stress and neuroinflammation in diabetic cognitive dysfunction.
Article Snippet: This is a PDF of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability.. This version will undergo additional copyediting, typesetting and review before it is published in its final form.. As such, this version is no longer the Accepted Manuscript, but it is not yet the definitive Version of Record; we are providing this early version to give early visibility of the article.

Cycling Probe Technology:

Article Title: Senolytic Interventions Enhance the Anti-metastatic Activity of Chemotherapy in Prostate Cancer
Article Snippet: PF-06873600 (ebvaciclib, A16875) was purchased from Adooq Biosciences. .. Docetaxel (RP-56976, HY-B0011), irinotecan (CPT-11, S1198), LCL161 (HY-15518), and MCC950 (HY-12815) were purchased from MedChemExpress. .. Necrostatin-1 (Nec-1;2324) was purchased from Bio-techne Tocris.

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Journal: Journal of Diabetes Research

Article Title: The AGEs/RAGE Axis Contributes to Myocardial Cell Death in Type 1 Diabetic Cardiomyopathy via the ROS/NF‐ κ B/NLRP3 Inflammasome Pathway

doi: 10.1155/jdr/6438008

Figure Lengend Snippet: AGEs activate the NLRP3 inflammasome in cardiomyocytes via the RAGE/ROS/NF‐ κ B signaling axis. (a–k) Primary neonatal mouse cardiomyocytes were pretreated with or without the RAGE inhibitor FPS‐ZM1 (20 μ M) or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (a) Representative Western blots of phospho‐NF‐ κ B p65 (pp65), total NF‐ κ B p65, NLRP3, caspase‐1 P20, and N‐GSDMD. (b–e) Quantitative analysis of the protein levels of (b) pp65/NF‐ κ B p65, (c) NLRP3, (d) caspase‐1 P20, and (e) N‐GSDMD, n = 4. (f,g) Concentrations of (f) I L‐1 β and (g) IL‐18 in the cell culture supernatant were measured by ELISA, n = 4. (h,i) Intracellular ROS levels were detected using the DCFHDA fluorescent probe. (h) Representative fluorescence images. Scale bar, 50 μ m. (i) Quantitative analysis of ROS fluorescence intensity, n = 4. (j,k) ASC oligomerization was assessed by immunofluorescence. (j) Representative images showing ASC specks. Scale bar, 10 μ m. (k) Quantification of ASC fluorescence intensity, n = 4. (l–v) Cardiomyocytes were pretreated with or without the ROS scavenger NAC (10 μ M) or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (l) Representative immunoblots of the indicated proteins. (m–p) Quantitative analysis of (m) pp65/NF‐ κ B p65, (n) NLRP3, (o) caspase‐1 P20, and (p) N‐GSDMD, n = 4. (q,r) ELISA analysis of (q) IL‐1 β and (r) IL‐18 levels in the supernatant, n = 4. (s,t) Intracellular ROS levels were measured as above. (s) Representative images. Scale bar, 50 μ m. (T) Fluorescence quantification, n = 4. (u,v) Assessment of ASC speck formation. (u) Representative images. Scale bar, 10 μ m. (v) Quantification of ASC fluorescence intensity, n = 4.

Article Snippet: FPS‐ZM1 and MCC950 (Cat#HY‐19370 and Cat#HY‐12815), STZ (Cat#HY‐13753) were obtained from MedChemExpress (Shanghai, China).

Techniques: Western Blot, Analysis, Cell Culture, Enzyme-linked Immunosorbent Assay, Fluorescence, Immunofluorescence

Journal: Journal of Diabetes Research

Article Title: The AGEs/RAGE Axis Contributes to Myocardial Cell Death in Type 1 Diabetic Cardiomyopathy via the ROS/NF‐ κ B/NLRP3 Inflammasome Pathway

doi: 10.1155/jdr/6438008

Figure Lengend Snippet: AGEs induce pyroptotic cell death in cardiomyocytes through the RAGE/ROS/NLRP3 pathway. Primary neonatal mouse cardiomyocytes were pretreated with or without FPS‐ZM1 (20 μ M), NAC (10 μ M), MCC950 (10 μ M), or vehicle for 1 h, followed by stimulation with AGEs (200 μ g/mL) for 24 h. (a) Representative fluorescence images of SYTOX green staining. Scale bar, 200 μ m. (b) Quantitative analysis of SYTOX‐positive cells, n = 4. (c) Representative fluorescence images of propidium iodide (PI) uptake. Scale bar, 100 μ m. (d) Quantitative analysis of PI‐positive cells, n = 4. (e) Lactate dehydrogenase (LDH) release in the cell culture supernatant was measured, n = 4.

Article Snippet: FPS‐ZM1 and MCC950 (Cat#HY‐19370 and Cat#HY‐12815), STZ (Cat#HY‐13753) were obtained from MedChemExpress (Shanghai, China).

Techniques: Fluorescence, Staining, Analysis, Cell Culture

C1qc mediates the effects of migrasomes on the BBB via the Nlrp3–Caspase 1–GSDMD pathway. (A) Immunoblots revealed C1qc, Nlrp3, cleaved caspase‐1, and GSDMD‐N protein expression levels in C1qc flox/flox model mice injected with AAV–Iba1–Cre or AAV–con ( n = 5). Densitometric quantification of protein levels; the data are presented as the mean SD; ** p < 0.01, *** p < 0.001, **** p < 0.0001. (B) Immunofluorescence staining for GSDMD–N and the endothelial cell marker CD31 in the perihaematomal area of C1qc flox/flox model mice injected with AAV–Iba1–Cre or AAV–con ( n = 5). Normalized quantitative measurement of GSDMD‐N fluorescence intensity relative to CD31 area. The data are presented as the mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (C) Immunofluorescence staining for cleaved caspase‐1 and the endothelial cell marker CD31 in the perihaematomal area of C1qc flox/flox model mice injected with AAV–Iba1–Cre or AAV–con ( n = 5). Fluorescence signal density from cleaved caspase‐1, normalized against the CD31 area, was analysed quantitatively. The data are expressed as ± SD; *** p < 0.001, **** p < 0.0001. (D) GSDMD‐N staining of endothelial cells that were treated as described in Figure ( n = 3). Quantification of the fluorescence intensity of GSDMD‐N of endothelial cells in the vehicle + microglia‐secreting migrasome group, the hemin + microglia‐secreting migrasome group, and the hemin + siC1qc microglia‐secreting migrasome group were also quantified. Data are presented as the mean ± SD with the indicated significance, * p < 0.05, ** p < 0.01, *** p < 0.001. (E) Cleaved caspase‐1 staining of endothelial cells that were treated as described previously in Figure ( n = 3). Quantification of the fluorescence intensity of Cleaved caspase‐1 of endothelial cells in the vehicle + microglial migrasome groups, hemin + microglial migrasome group, and hemin + siC1qc microglial migrasome group were also quantified. The data are presented as the means ± SDs; * p < 0.05, ** p < 0.01. (F) Immunoblots showing the levels of the Nlrp3 and GAPDH proteins in endothelial cells that were treated as described in Figure ( n = 6). Densitometric quantification of protein levels. The data are presented as the mean ± SD; *** p < 0.001. (G) Claudin‐5 staining of endothelial cells that were treated with MCC950 and microglial migrasomes without C1qc ( n = 5). Quantification of the fluorescence intensity of Claudin‐5. The data are presented as the mean ± SD; ns, no significant difference; ** p < 0.01, *** p < 0.001. (H) GSDMD‐N immunofluorescence in endothelial cells treated with migrasomes, C1qc‐deficient migrasomes, or C1qc‐deficient migrasomes plus Nigericin. Quantification of the fluorescence intensity of GSDMD‐N. The data are presented as the mean ± SD; ** p < 0.01, *** p < 0.001. (I) Claudin‐5 immunofluorescence in endothelial cells treated with migrasomes, C1qc‐deficient migrasomes, or C1qc‐deficient migrasomes plus Nigericin. Quantification of the fluorescence intensity of Claudin‐5. The data are presented as the mean ± SD; * p < 0.05, *** p < 0.001. (J) Immunoblots showing the levels of the GSDMD‐N, Claudin‐5 and GAPDH proteins in endothelial cells that were treated with migrasomes at different time points ( n = 6). Densitometric quantification of protein levels. The data are presented as the mean ± SD; ns = no significant difference, ** p < 0.01, *** p < 0.001. (K) Cell viability dramatically decreased endothelial cells that were treated with migrasomes at different time points ( n = 3). Data are shown as the means ± SD with significance levels; ns = no significant difference, * p < 0.05, *** p < 0.001, **** p < 0.0001.

Journal: Journal of Extracellular Vesicles

Article Title: C1qc Mediates Blood–Brain Barrier Disruption in a Mouse Model of Intracerebral Haemorrhage Through Microglia‐Derived Migrasomes

doi: 10.1002/jev2.70377

Figure Lengend Snippet: C1qc mediates the effects of migrasomes on the BBB via the Nlrp3–Caspase 1–GSDMD pathway. (A) Immunoblots revealed C1qc, Nlrp3, cleaved caspase‐1, and GSDMD‐N protein expression levels in C1qc flox/flox model mice injected with AAV–Iba1–Cre or AAV–con ( n = 5). Densitometric quantification of protein levels; the data are presented as the mean SD; ** p < 0.01, *** p < 0.001, **** p < 0.0001. (B) Immunofluorescence staining for GSDMD–N and the endothelial cell marker CD31 in the perihaematomal area of C1qc flox/flox model mice injected with AAV–Iba1–Cre or AAV–con ( n = 5). Normalized quantitative measurement of GSDMD‐N fluorescence intensity relative to CD31 area. The data are presented as the mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. (C) Immunofluorescence staining for cleaved caspase‐1 and the endothelial cell marker CD31 in the perihaematomal area of C1qc flox/flox model mice injected with AAV–Iba1–Cre or AAV–con ( n = 5). Fluorescence signal density from cleaved caspase‐1, normalized against the CD31 area, was analysed quantitatively. The data are expressed as ± SD; *** p < 0.001, **** p < 0.0001. (D) GSDMD‐N staining of endothelial cells that were treated as described in Figure ( n = 3). Quantification of the fluorescence intensity of GSDMD‐N of endothelial cells in the vehicle + microglia‐secreting migrasome group, the hemin + microglia‐secreting migrasome group, and the hemin + siC1qc microglia‐secreting migrasome group were also quantified. Data are presented as the mean ± SD with the indicated significance, * p < 0.05, ** p < 0.01, *** p < 0.001. (E) Cleaved caspase‐1 staining of endothelial cells that were treated as described previously in Figure ( n = 3). Quantification of the fluorescence intensity of Cleaved caspase‐1 of endothelial cells in the vehicle + microglial migrasome groups, hemin + microglial migrasome group, and hemin + siC1qc microglial migrasome group were also quantified. The data are presented as the means ± SDs; * p < 0.05, ** p < 0.01. (F) Immunoblots showing the levels of the Nlrp3 and GAPDH proteins in endothelial cells that were treated as described in Figure ( n = 6). Densitometric quantification of protein levels. The data are presented as the mean ± SD; *** p < 0.001. (G) Claudin‐5 staining of endothelial cells that were treated with MCC950 and microglial migrasomes without C1qc ( n = 5). Quantification of the fluorescence intensity of Claudin‐5. The data are presented as the mean ± SD; ns, no significant difference; ** p < 0.01, *** p < 0.001. (H) GSDMD‐N immunofluorescence in endothelial cells treated with migrasomes, C1qc‐deficient migrasomes, or C1qc‐deficient migrasomes plus Nigericin. Quantification of the fluorescence intensity of GSDMD‐N. The data are presented as the mean ± SD; ** p < 0.01, *** p < 0.001. (I) Claudin‐5 immunofluorescence in endothelial cells treated with migrasomes, C1qc‐deficient migrasomes, or C1qc‐deficient migrasomes plus Nigericin. Quantification of the fluorescence intensity of Claudin‐5. The data are presented as the mean ± SD; * p < 0.05, *** p < 0.001. (J) Immunoblots showing the levels of the GSDMD‐N, Claudin‐5 and GAPDH proteins in endothelial cells that were treated with migrasomes at different time points ( n = 6). Densitometric quantification of protein levels. The data are presented as the mean ± SD; ns = no significant difference, ** p < 0.01, *** p < 0.001. (K) Cell viability dramatically decreased endothelial cells that were treated with migrasomes at different time points ( n = 3). Data are shown as the means ± SD with significance levels; ns = no significant difference, * p < 0.05, *** p < 0.001, **** p < 0.0001.

Article Snippet: Ten milligrams of the inflammasome inhibitor MCC950 (Nlrp3 inhibitor)(Selleck Chemicals, Houston, TX, USA) was dissolved in 1 mL of 1× phosphate‐buffered saline (PBS).

Techniques: Western Blot, Expressing, Injection, Immunofluorescence, Staining, Marker, Fluorescence

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mcc950 (MedChemExpress)

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1) Product Images from "The AGEs/RAGE Axis Contributes to Myocardial Cell Death in Type 1 Diabetic Cardiomyopathy via the ROS/NF‐ κ B/NLRP3 Inflammasome Pathway"

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