Review

activator ns19504 (Alomone Labs)

Alomone Labs is a verified supplier

Alomone Labs manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Alomone Labs activator ns19504

BK channel activator <t>NS19504</t> promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p < 0.05, control vs. NS19504 or Paxilline vs. NS19504 group. (C) Representative photomicrographs showed that neuronal debris (red) phagocytosed by microglia (green) in the NS19504- and Paxilline-treated mice following tMCAO. Scale bar = 25 μm. (D) Bar graph shows semiquantitative data of the proportion of microglia that phagocytose neuronal debris. Data are mean + SE, n = 3 per group. * p < 0.05, NS19504 vs. control or Paxilline vs. NS19504 group. (E) Representative photomicrographs show FITC and PE-positive cells. FITC-labeled beads were phagocytosed by PE-labeled microglia. Primary microglia were divided into the control group (basic microglia medium); LPS group (200 ng/ml LPS); LPS + NS19504 group (200 ng/ml LPS and 10 μM NS19504); and LPS + Paxilline group (200 ng/ml LPS and 1 μM Paxilline). (F) Bar graph shows semiquantitative analysis of the proportion of microglia that phagocytose beads. Data are mean + SE, n = 3 per group. ** p < 0.01, compared with the control group. # p < 0.05, compared with the Paxilline group. (G) Bar graph shows the result of CCK-8 assay in the primary microglia without or with different concentrations of Paxilline and NS19504 for 12 h of OGD. Data are mean ± SE, n = 3 per group. # p < 0.05, ## p < 0.01, compared with the control group. * p < 0.05, ** p < 0.01; NS represents for NS19504, and Pax represents for Paxilline.

Activator Ns19504, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/activator+ns19504/pmc08281043-72-9-14?v=Alomone+Labs
Average 93 stars, based on 1 article reviews

activator ns19504 - by Bioz Stars, 2026-07

93/100 stars

Images

1) Product Images from "BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke"

Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

Journal: Frontiers in Cellular Neuroscience

doi: 10.3389/fncel.2021.683769

BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p < 0.05, control vs. NS19504 or Paxilline vs. NS19504 group. (C) Representative photomicrographs showed that neuronal debris (red) phagocytosed by microglia (green) in the NS19504- and Paxilline-treated mice following tMCAO. Scale bar = 25 μm. (D) Bar graph shows semiquantitative data of the proportion of microglia that phagocytose neuronal debris. Data are mean + SE, n = 3 per group. * p < 0.05, NS19504 vs. control or Paxilline vs. NS19504 group. (E) Representative photomicrographs show FITC and PE-positive cells. FITC-labeled beads were phagocytosed by PE-labeled microglia. Primary microglia were divided into the control group (basic microglia medium); LPS group (200 ng/ml LPS); LPS + NS19504 group (200 ng/ml LPS and 10 μM NS19504); and LPS + Paxilline group (200 ng/ml LPS and 1 μM Paxilline). (F) Bar graph shows semiquantitative analysis of the proportion of microglia that phagocytose beads. Data are mean + SE, n = 3 per group. ** p < 0.01, compared with the control group. # p < 0.05, compared with the Paxilline group. (G) Bar graph shows the result of CCK-8 assay in the primary microglia without or with different concentrations of Paxilline and NS19504 for 12 h of OGD. Data are mean ± SE, n = 3 per group. # p < 0.05, ## p < 0.01, compared with the control group. * p < 0.05, ** p < 0.01; NS represents for NS19504, and Pax represents for Paxilline.

Figure Legend Snippet: BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p < 0.05, control vs. NS19504 or Paxilline vs. NS19504 group. (C) Representative photomicrographs showed that neuronal debris (red) phagocytosed by microglia (green) in the NS19504- and Paxilline-treated mice following tMCAO. Scale bar = 25 μm. (D) Bar graph shows semiquantitative data of the proportion of microglia that phagocytose neuronal debris. Data are mean + SE, n = 3 per group. * p < 0.05, NS19504 vs. control or Paxilline vs. NS19504 group. (E) Representative photomicrographs show FITC and PE-positive cells. FITC-labeled beads were phagocytosed by PE-labeled microglia. Primary microglia were divided into the control group (basic microglia medium); LPS group (200 ng/ml LPS); LPS + NS19504 group (200 ng/ml LPS and 10 μM NS19504); and LPS + Paxilline group (200 ng/ml LPS and 1 μM Paxilline). (F) Bar graph shows semiquantitative analysis of the proportion of microglia that phagocytose beads. Data are mean + SE, n = 3 per group. ** p < 0.01, compared with the control group. # p < 0.05, compared with the Paxilline group. (G) Bar graph shows the result of CCK-8 assay in the primary microglia without or with different concentrations of Paxilline and NS19504 for 12 h of OGD. Data are mean ± SE, n = 3 per group. # p < 0.05, ## p < 0.01, compared with the control group. * p < 0.05, ** p < 0.01; NS represents for NS19504, and Pax represents for Paxilline.

Techniques Used: Control, Cell Culture, Labeling, CCK-8 Assay

Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p < 0.01. (C) Representative photomicrograms of NeuN + neurons (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (D) Bar graph shows quantitative analysis of the number of NeuN + /TUNEL + cells per vision. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p < 0.01.

Figure Legend Snippet: Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p < 0.01. (C) Representative photomicrograms of NeuN + neurons (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (D) Bar graph shows quantitative analysis of the number of NeuN + /TUNEL + cells per vision. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p < 0.01.

Techniques Used: Activation Assay, TUNEL Assay, Slice Preparation

Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p < 0.01. # NS19504 vs. DMSO, # p < 0.05.

Figure Legend Snippet: Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p < 0.01. # NS19504 vs. DMSO, # p < 0.05.

Techniques Used: Activation Assay, Modification

Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p < 0.05; ns, no significance.

Figure Legend Snippet: Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p < 0.05; ns, no significance.

Techniques Used: Western Blot

Image Search Results

Journal: Frontiers in Cellular Neuroscience

Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

doi: 10.3389/fncel.2021.683769

Figure Lengend Snippet: BK channel activator NS19504 promoted microglial phagocytosis after OGD in primary culture . (A) Representative images of beads (red) phagocytosed by CD11b + microglia (green) after 1 h of OGD. Control group: primary microglia cultured with basic microglia medium; NS19504 group: primary microglia cultured with 10 μM NS19504 in basic microglia medium; Paxilline group: primary microglia cultured with 1 μM Paxilline in basic microglia medium. Scale bar = 25 μm. (B) Bar graph showed that semiquantitative data of the relative bead density versus microglia. Data are mean + SE, n = 3 per group. * p < 0.05, control vs. NS19504 or Paxilline vs. NS19504 group. (C) Representative photomicrographs showed that neuronal debris (red) phagocytosed by microglia (green) in the NS19504- and Paxilline-treated mice following tMCAO. Scale bar = 25 μm. (D) Bar graph shows semiquantitative data of the proportion of microglia that phagocytose neuronal debris. Data are mean + SE, n = 3 per group. * p < 0.05, NS19504 vs. control or Paxilline vs. NS19504 group. (E) Representative photomicrographs show FITC and PE-positive cells. FITC-labeled beads were phagocytosed by PE-labeled microglia. Primary microglia were divided into the control group (basic microglia medium); LPS group (200 ng/ml LPS); LPS + NS19504 group (200 ng/ml LPS and 10 μM NS19504); and LPS + Paxilline group (200 ng/ml LPS and 1 μM Paxilline). (F) Bar graph shows semiquantitative analysis of the proportion of microglia that phagocytose beads. Data are mean + SE, n = 3 per group. ** p < 0.01, compared with the control group. # p < 0.05, compared with the Paxilline group. (G) Bar graph shows the result of CCK-8 assay in the primary microglia without or with different concentrations of Paxilline and NS19504 for 12 h of OGD. Data are mean ± SE, n = 3 per group. # p < 0.05, ## p < 0.01, compared with the control group. * p < 0.05, ** p < 0.01; NS represents for NS19504, and Pax represents for Paxilline.

Article Snippet: The selective BK channel antagonist Paxilline ( ) and activator NS19504 ( ) powder (Alomone Labs, Jerusalem, Israel) were, respectively, dissolved in DMSO to the final storage concentrations of 2 and 50 mM.

Techniques: Control, Cell Culture, Labeling, CCK-8 Assay

Journal: Frontiers in Cellular Neuroscience

Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

doi: 10.3389/fncel.2021.683769

Figure Lengend Snippet: Activation of BK channels promoted the phagocytic function of microglia after tMCAO and decreased neuronal apoptosis . (A) Representative photomicrograms of IBA1 + microglia (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (B) Bar graph shows quantitative analysis of the number of IBA1 + TUNEL + cells per field. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p < 0.01. (C) Representative photomicrograms of NeuN + neurons (green) and TUNEL + apoptotic cells (red) in the peri-infarct region of brain slice in the DMSO, NS19504, and Paxilline groups at 3 days after tMCAO. Scale bar = 50 μm. (D) Bar graph shows quantitative analysis of the number of NeuN + /TUNEL + cells per vision. Data are mean + SE, n = 3 per group. *vs. DMSO group, ** p < 0.01.

Techniques: Activation Assay, TUNEL Assay, Slice Preparation

Journal: Frontiers in Cellular Neuroscience

Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

doi: 10.3389/fncel.2021.683769

Figure Lengend Snippet: Activation of BK channels ameliorated stroke outcomes. (A) Experiment design of the animal experiment. Three days before tMCAO, mice were subjected behavior training. After a 90-min tMCAO surgery, mice were divided randomly into four groups (sham, DMSO, NS19504, and Paxilline). At 1, 3, 7, and 14 days, behavior tests were performed, and protein and RNA samples were collected. (B) Weight changes of mice in three groups at 1, 2, 3, 7, and 14 days after tMCAO. (C) Modified Neurological Severity Score of three groups at 1, 3, 7, and 14 days after tMCAO. (D) Average score per second of three groups of hinging wire at 3 days after tMCAO. (E) Survivorship curve during 14 days of three groups after tMCAO. Data are mean + SE, n = 21–23 per group at 1 day, n = 17–23 per group at 3 days, n = 8–13 per group at 7 days, n = 3–9 per group at 14 days. *NS19504 vs. Paxilline group, ** p < 0.01. # NS19504 vs. DMSO, # p < 0.05.

Techniques: Activation Assay, Modification

Journal: Frontiers in Cellular Neuroscience

Article Title: BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke

doi: 10.3389/fncel.2021.683769

Figure Lengend Snippet: Inflammatory factors and phosphorylated-ERK expressions under different treatments at 3 days after tMCAO . (A) Bar graph represents the relative mRNA levels of inflammatory factors including TNF-α, TGF-β, IL-10, IL-6, IL-1β, and IL-1α. Data are mean + SE, n = 3 per group. (B) Representative image of Western blot of phosphorylated-ERK1/2 (p-ERK), total-ERK1/2 (t-ERK), and β-actin at 3 days after tMCAO. (C) Bar graph showing the relative protein levels of p -ERK vs. t-ERK at 3 day after tMCAO. Data are mean + SE, n = 9 per group. *NS19504 vs. Paxilline group, * p < 0.05; ns, no significance.

Techniques: Western Blot

Review

Structured Review

Images

1) Product Images from "BK Channel-Mediated Microglial Phagocytosis Alleviates Neurological Deficit After Ischemic Stroke"

Similar Products

Image Search Results