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Associations of individual inflammation marker or combination of IL-6 and YKL-40 with recurrent stroke within 1 year
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Associations of individual inflammation marker or combination of IL-6 and YKL-40 with recurrent stroke within 1 year
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Roles of NF‐κB and MAPK pathways in regulating inflammatory cytokine secretion in linarin‐treated cells. (A, B) hNECs and BEAS‐2B cells were treated with dexamethasone (100 nM) or the inhibitors of NF‐κB (PDTC, 10 μM), ERK (U0126, 10 μM), JNK (SP600125, 10 μM), and p38 (SB203580, 30 μM) for 24 h. The cytotoxicity effects of dexamethasone and these inhibitors were evaluated by CCK‐8 assay. (C–H) hNECs and BEAS‐2B cells were pretreated with linarin or/and the inhibitors of NF‐κB (PDTC, 10 μM), ERK (U0126, 10 μM), JNK (SP600125, 10 μM), and p38 (SB203580, 30 μM) for 1 h, and then stimulated with histamine (100 μM) for 24 h. The secretion levels of <t>IL‐6,</t> IL‐8, and MCP‐1 in the medium were detected by ELISA. Cells pretreated with dexamethasone (100 nM) for 1 h and then stimulated with histamine (100 μM) for 24 h were used as a positive control. * p < 0.05, ** p < 0.01, and *** p < 0.001 versus relative group. SP, SP600125. SB, SB203580. Dex, dexamethasone.
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Roles of NF‐κB and MAPK pathways in regulating inflammatory cytokine secretion in linarin‐treated cells. (A, B) hNECs and BEAS‐2B cells were treated with dexamethasone (100 nM) or the inhibitors of NF‐κB (PDTC, 10 μM), ERK (U0126, 10 μM), JNK (SP600125, 10 μM), and p38 (SB203580, 30 μM) for 24 h. The cytotoxicity effects of dexamethasone and these inhibitors were evaluated by CCK‐8 assay. (C–H) hNECs and BEAS‐2B cells were pretreated with linarin or/and the inhibitors of NF‐κB (PDTC, 10 μM), ERK (U0126, 10 μM), JNK (SP600125, 10 μM), and p38 (SB203580, 30 μM) for 1 h, and then stimulated with histamine (100 μM) for 24 h. The secretion levels of <t>IL‐6,</t> IL‐8, and MCP‐1 in the medium were detected by ELISA. Cells pretreated with dexamethasone (100 nM) for 1 h and then stimulated with histamine (100 μM) for 24 h were used as a positive control. * p < 0.05, ** p < 0.01, and *** p < 0.001 versus relative group. SP, SP600125. SB, SB203580. Dex, dexamethasone.
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ZQG attenuates PMA-induced NETosis and inflammatory responses in human neutrophils via targeting the Nox4/ROS pathway. (A) ZQG suppresses oxidative burst and NET formation. Representative immunofluorescence images showing intracellular ROS (stained by DHE, red) and NETosis (marked by CitH3, green). Nuclei are counterstained with DAPI (blue). Scale bars: 20 μm. (B) Quantitative analysis of intracellular ROS levels. (C) Quantification of NETosis, expressed as the percentage of Sytox Green + cells. (D) Western blot analysis demonstrating the effects of ZQG and si-Nox4 on the protein expression of Nox4, p-Akt, and PADI4. (E) Densitometric quantification of Western blot results. (F) qPCR analysis of Nox4, PI3K, Akt, and PADI4 mRNA expression. (G) <t>ELISA</t> analysis of pro-inflammatory cytokine levels (IL-2, IL-5, IL-6, <t>IL-12,</t> <t>TNF-α)</t> in cell culture supernatants. Data are presented as mean ± SEM (n=10 independent experiments). ***p < 0.001 vs. PMA group.
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ZQG attenuates PMA-induced NETosis and inflammatory responses in human neutrophils via targeting the Nox4/ROS pathway. (A) ZQG suppresses oxidative burst and NET formation. Representative immunofluorescence images showing intracellular ROS (stained by DHE, red) and NETosis (marked by CitH3, green). Nuclei are counterstained with DAPI (blue). Scale bars: 20 μm. (B) Quantitative analysis of intracellular ROS levels. (C) Quantification of NETosis, expressed as the percentage of Sytox Green + cells. (D) Western blot analysis demonstrating the effects of ZQG and si-Nox4 on the protein expression of Nox4, p-Akt, and PADI4. (E) Densitometric quantification of Western blot results. (F) qPCR analysis of Nox4, PI3K, Akt, and PADI4 mRNA expression. (G) <t>ELISA</t> analysis of pro-inflammatory cytokine levels (IL-2, IL-5, IL-6, <t>IL-12,</t> <t>TNF-α)</t> in cell culture supernatants. Data are presented as mean ± SEM (n=10 independent experiments). ***p < 0.001 vs. PMA group.
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ZQG attenuates PMA-induced NETosis and inflammatory responses in human neutrophils via targeting the Nox4/ROS pathway. (A) ZQG suppresses oxidative burst and NET formation. Representative immunofluorescence images showing intracellular ROS (stained by DHE, red) and NETosis (marked by CitH3, green). Nuclei are counterstained with DAPI (blue). Scale bars: 20 μm. (B) Quantitative analysis of intracellular ROS levels. (C) Quantification of NETosis, expressed as the percentage of Sytox Green + cells. (D) Western blot analysis demonstrating the effects of ZQG and si-Nox4 on the protein expression of Nox4, p-Akt, and PADI4. (E) Densitometric quantification of Western blot results. (F) qPCR analysis of Nox4, PI3K, Akt, and PADI4 mRNA expression. (G) <t>ELISA</t> analysis of pro-inflammatory cytokine levels (IL-2, IL-5, IL-6, <t>IL-12,</t> <t>TNF-α)</t> in cell culture supernatants. Data are presented as mean ± SEM (n=10 independent experiments). ***p < 0.001 vs. PMA group.
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Image Search Results


Associations of individual inflammation marker or combination of IL-6 and YKL-40 with recurrent stroke within 1 year

Journal: Journal of Neuroinflammation

Article Title: Interleukin-6 and YKL-40 predicted recurrent stroke after ischemic stroke or TIA: analysis of 6 inflammation biomarkers in a prospective cohort study

doi: 10.1186/s12974-022-02467-1

Figure Lengend Snippet: Associations of individual inflammation marker or combination of IL-6 and YKL-40 with recurrent stroke within 1 year

Article Snippet: The concentrations of IL-6, IL-1Ra, Lp-PLA 2 and YKL-40 were determined by using enzyme-linked immunosorbent assay kits (catalogue number: PHS600C for IL-6, PDRA00B for IL-1Ra, DPLG70 for Lp-PLA 2 and DC3L10 for YKL-40, R&D Systems, Inc, Minneapolis, MN, USA).

Techniques: Marker

Associations of individual inflammation marker or combination of IL-6 and YKL-40 with a Modified Rankin Scale score ≥ 2 within 1 year

Journal: Journal of Neuroinflammation

Article Title: Interleukin-6 and YKL-40 predicted recurrent stroke after ischemic stroke or TIA: analysis of 6 inflammation biomarkers in a prospective cohort study

doi: 10.1186/s12974-022-02467-1

Figure Lengend Snippet: Associations of individual inflammation marker or combination of IL-6 and YKL-40 with a Modified Rankin Scale score ≥ 2 within 1 year

Article Snippet: The concentrations of IL-6, IL-1Ra, Lp-PLA 2 and YKL-40 were determined by using enzyme-linked immunosorbent assay kits (catalogue number: PHS600C for IL-6, PDRA00B for IL-1Ra, DPLG70 for Lp-PLA 2 and DC3L10 for YKL-40, R&D Systems, Inc, Minneapolis, MN, USA).

Techniques: Marker, Modification

Roles of NF‐κB and MAPK pathways in regulating inflammatory cytokine secretion in linarin‐treated cells. (A, B) hNECs and BEAS‐2B cells were treated with dexamethasone (100 nM) or the inhibitors of NF‐κB (PDTC, 10 μM), ERK (U0126, 10 μM), JNK (SP600125, 10 μM), and p38 (SB203580, 30 μM) for 24 h. The cytotoxicity effects of dexamethasone and these inhibitors were evaluated by CCK‐8 assay. (C–H) hNECs and BEAS‐2B cells were pretreated with linarin or/and the inhibitors of NF‐κB (PDTC, 10 μM), ERK (U0126, 10 μM), JNK (SP600125, 10 μM), and p38 (SB203580, 30 μM) for 1 h, and then stimulated with histamine (100 μM) for 24 h. The secretion levels of IL‐6, IL‐8, and MCP‐1 in the medium were detected by ELISA. Cells pretreated with dexamethasone (100 nM) for 1 h and then stimulated with histamine (100 μM) for 24 h were used as a positive control. * p < 0.05, ** p < 0.01, and *** p < 0.001 versus relative group. SP, SP600125. SB, SB203580. Dex, dexamethasone.

Journal: The Kaohsiung Journal of Medical Sciences

Article Title: In Vitro Evaluation of the Inhibitory Effects of Linarin on Histamine‐Induced Expression of Proinflammatory Cytokines, Mucin 5AC , and Aquaporin 5 in Human Nasal and Bronchial Epithelial Cells

doi: 10.1002/kjm2.70114

Figure Lengend Snippet: Roles of NF‐κB and MAPK pathways in regulating inflammatory cytokine secretion in linarin‐treated cells. (A, B) hNECs and BEAS‐2B cells were treated with dexamethasone (100 nM) or the inhibitors of NF‐κB (PDTC, 10 μM), ERK (U0126, 10 μM), JNK (SP600125, 10 μM), and p38 (SB203580, 30 μM) for 24 h. The cytotoxicity effects of dexamethasone and these inhibitors were evaluated by CCK‐8 assay. (C–H) hNECs and BEAS‐2B cells were pretreated with linarin or/and the inhibitors of NF‐κB (PDTC, 10 μM), ERK (U0126, 10 μM), JNK (SP600125, 10 μM), and p38 (SB203580, 30 μM) for 1 h, and then stimulated with histamine (100 μM) for 24 h. The secretion levels of IL‐6, IL‐8, and MCP‐1 in the medium were detected by ELISA. Cells pretreated with dexamethasone (100 nM) for 1 h and then stimulated with histamine (100 μM) for 24 h were used as a positive control. * p < 0.05, ** p < 0.01, and *** p < 0.001 versus relative group. SP, SP600125. SB, SB203580. Dex, dexamethasone.

Article Snippet: The levels of IL‐6, IL‐8, and MCP‐1 were determined using a Human IL‐6 Quantikine ELISA Kit (QK206; R&D Systems, Minneapolis, MN), Human IL‐8/CXCL8 Quantikine ELISA Kit (D8000C; R&D Systems), and Human CCL2/MCP‐1 Quantikine ELISA Kit (DCP00; R&D Systems) following the manufacturer's protocol.

Techniques: CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Positive Control

ZQG attenuates PMA-induced NETosis and inflammatory responses in human neutrophils via targeting the Nox4/ROS pathway. (A) ZQG suppresses oxidative burst and NET formation. Representative immunofluorescence images showing intracellular ROS (stained by DHE, red) and NETosis (marked by CitH3, green). Nuclei are counterstained with DAPI (blue). Scale bars: 20 μm. (B) Quantitative analysis of intracellular ROS levels. (C) Quantification of NETosis, expressed as the percentage of Sytox Green + cells. (D) Western blot analysis demonstrating the effects of ZQG and si-Nox4 on the protein expression of Nox4, p-Akt, and PADI4. (E) Densitometric quantification of Western blot results. (F) qPCR analysis of Nox4, PI3K, Akt, and PADI4 mRNA expression. (G) ELISA analysis of pro-inflammatory cytokine levels (IL-2, IL-5, IL-6, IL-12, TNF-α) in cell culture supernatants. Data are presented as mean ± SEM (n=10 independent experiments). ***p < 0.001 vs. PMA group.

Journal: Frontiers in Immunology

Article Title: Pathological neutrophil extracellular traps hinder postoperative anal fistula wound healing and are attenuated by Zuoqing granule via suppression of the Nox4 pathway

doi: 10.3389/fimmu.2025.1730184

Figure Lengend Snippet: ZQG attenuates PMA-induced NETosis and inflammatory responses in human neutrophils via targeting the Nox4/ROS pathway. (A) ZQG suppresses oxidative burst and NET formation. Representative immunofluorescence images showing intracellular ROS (stained by DHE, red) and NETosis (marked by CitH3, green). Nuclei are counterstained with DAPI (blue). Scale bars: 20 μm. (B) Quantitative analysis of intracellular ROS levels. (C) Quantification of NETosis, expressed as the percentage of Sytox Green + cells. (D) Western blot analysis demonstrating the effects of ZQG and si-Nox4 on the protein expression of Nox4, p-Akt, and PADI4. (E) Densitometric quantification of Western blot results. (F) qPCR analysis of Nox4, PI3K, Akt, and PADI4 mRNA expression. (G) ELISA analysis of pro-inflammatory cytokine levels (IL-2, IL-5, IL-6, IL-12, TNF-α) in cell culture supernatants. Data are presented as mean ± SEM (n=10 independent experiments). ***p < 0.001 vs. PMA group.

Article Snippet: The concentrations of interleukin-2 (IL-2), interleukin-5 (IL-5), interleukin-6 (IL-6), interleukin-12 (IL-12), and tumor necrosis factor-alpha (TNF-α) in the supernatants were quantified using specific commercial rat ELISA kits (R&D Systems, Catalog # R6000B) according to the manufacturers’ instructions.

Techniques: Immunofluorescence, Staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Cell Culture