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human gingival fibroblast hgf 1  (ATCC)


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    Structured Review

    ATCC human gingival fibroblast hgf 1
    Cytotoxicity of CAP treatment <t>in</t> <t>HGF-1</t> cells. Cell viability was assessed after CAP exposure at 6 and 24 h using the WST-8 assay. (A) 25–25 condition, (B) 50–50 condition, and (C) 75–75 condition. CAP treatment up to 180 s maintained cell viability above ∼ 80%, with slight reductions observed at longer exposure times under higher power conditions. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, compared to the control of 6 h. # p < 0.05, ## p < 0.01, compared to the control of 24 h.
    Human Gingival Fibroblast Hgf 1, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1870 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human gingival fibroblast hgf 1/product/ATCC
    Average 96 stars, based on 1870 article reviews
    human gingival fibroblast hgf 1 - by Bioz Stars, 2026-02
    96/100 stars

    Images

    1) Product Images from "Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation"

    Article Title: Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation

    Journal: ACS Omega

    doi: 10.1021/acsomega.5c11346

    Cytotoxicity of CAP treatment in HGF-1 cells. Cell viability was assessed after CAP exposure at 6 and 24 h using the WST-8 assay. (A) 25–25 condition, (B) 50–50 condition, and (C) 75–75 condition. CAP treatment up to 180 s maintained cell viability above ∼ 80%, with slight reductions observed at longer exposure times under higher power conditions. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, compared to the control of 6 h. # p < 0.05, ## p < 0.01, compared to the control of 24 h.
    Figure Legend Snippet: Cytotoxicity of CAP treatment in HGF-1 cells. Cell viability was assessed after CAP exposure at 6 and 24 h using the WST-8 assay. (A) 25–25 condition, (B) 50–50 condition, and (C) 75–75 condition. CAP treatment up to 180 s maintained cell viability above ∼ 80%, with slight reductions observed at longer exposure times under higher power conditions. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, compared to the control of 6 h. # p < 0.05, ## p < 0.01, compared to the control of 24 h.

    Techniques Used: Control

    CAP-induced production of RONS in HGF-1 cells. (A–C) Extracellular levels of nitric oxide (NO), hydroxyl radicals ( • OH), and singlet oxygen ( 1 O 2 ) increased in a time- and power-dependent manner following CAP treatment (25–25, 50–50, and 75–75 conditions). (D) Intracellular ROS accumulation was measured by fluorescence microscopy at 6 and 24 h. (E) H 2 O 2 concentrations were significantly elevated in a time-dependent manner, and (F) CAP increased intracellular NO levels. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001 versus control.
    Figure Legend Snippet: CAP-induced production of RONS in HGF-1 cells. (A–C) Extracellular levels of nitric oxide (NO), hydroxyl radicals ( • OH), and singlet oxygen ( 1 O 2 ) increased in a time- and power-dependent manner following CAP treatment (25–25, 50–50, and 75–75 conditions). (D) Intracellular ROS accumulation was measured by fluorescence microscopy at 6 and 24 h. (E) H 2 O 2 concentrations were significantly elevated in a time-dependent manner, and (F) CAP increased intracellular NO levels. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001 versus control.

    Techniques Used: Fluorescence, Microscopy, Control

    Effects of 30 s CAP exposure on NF-κB, inflammatory cytokines, and COL1A1 expression in HGF-1 cells under various plasma discharge conditions. The mRNA expression levels of (A) NF-κB, (B) IL-6, (C) IL-1β, (D) TNF-α, and (E) COL1A1 were evaluated at 6 and 24 h after treatment. The data are shown as fold change relative to the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: Effects of 30 s CAP exposure on NF-κB, inflammatory cytokines, and COL1A1 expression in HGF-1 cells under various plasma discharge conditions. The mRNA expression levels of (A) NF-κB, (B) IL-6, (C) IL-1β, (D) TNF-α, and (E) COL1A1 were evaluated at 6 and 24 h after treatment. The data are shown as fold change relative to the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Expressing, Clinical Proteomics, Control

    CAP inhibits NF-κB signaling and the expression of pro-inflammatory cytokines in LPS-stimulated HGF-1 cells. (A) qRT-PCR results showing the relative mRNA expression levels of NF-κB, IL-6, IL-1β, and TNF-α in LPS-stimulated cells treated with CAP (30 or 60 s) or NAC. (B) Western blot analysis of NF-κB and phosphorylated NF-κB (p-NF-κB) demonstrating CAP’s suppression of NF-κB activation. (C) ELISA measurement of the amounts of IL-6, IL-1β, and TNF-α proteins in the culture supernatants. The data are shown as fold change compared with the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: CAP inhibits NF-κB signaling and the expression of pro-inflammatory cytokines in LPS-stimulated HGF-1 cells. (A) qRT-PCR results showing the relative mRNA expression levels of NF-κB, IL-6, IL-1β, and TNF-α in LPS-stimulated cells treated with CAP (30 or 60 s) or NAC. (B) Western blot analysis of NF-κB and phosphorylated NF-κB (p-NF-κB) demonstrating CAP’s suppression of NF-κB activation. (C) ELISA measurement of the amounts of IL-6, IL-1β, and TNF-α proteins in the culture supernatants. The data are shown as fold change compared with the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Expressing, Quantitative RT-PCR, Western Blot, Activation Assay, Enzyme-linked Immunosorbent Assay, Control

    CAP enhances the regenerative response of LPS-stimulated HGF-1 cells. (A) Exposure to CAP for 30 s promoted cell migration under LPS-induced inflammatory conditions. (B) Immunofluorescence staining of COL1A1 (green) revealed that CAP treatment stimulated collagen synthesis, while nuclei were counterstained with DAPI (blue). (C) Cell viability assays performed at 12 and 24 h post-treatment showed that CAP promoted HGF-1 cell proliferation under inflammatory conditions. The data are shown as fold change compared with the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.
    Figure Legend Snippet: CAP enhances the regenerative response of LPS-stimulated HGF-1 cells. (A) Exposure to CAP for 30 s promoted cell migration under LPS-induced inflammatory conditions. (B) Immunofluorescence staining of COL1A1 (green) revealed that CAP treatment stimulated collagen synthesis, while nuclei were counterstained with DAPI (blue). (C) Cell viability assays performed at 12 and 24 h post-treatment showed that CAP promoted HGF-1 cell proliferation under inflammatory conditions. The data are shown as fold change compared with the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Techniques Used: Migration, Immunofluorescence, Staining, Control

    Cold atmospheric plasma (CAP) restores mitochondrial function in LPS-stimulated HGF-1 cells. (A) CAP maintained mitochondrial membrane potential, evaluated via TMRM staining, in inflammatory conditions. 200× magnification. The scale bar is 50 μm. (B) CAP reduced mitochondrial ROS (mtROS) levels, as evidenced by MitoSOX Red fluorescence. The original magnification was 200×, and the scale bar was 50 μm. (C) Quantification of ATP production showed that CAP treatment (30 s) markedly increased cellular ATP levels compared with the LPS-only group and even exceeded those of the untreated control. (D) Immunofluorescence staining of HSP60 showed that the shape and content of mitochondria improved after CAP exposure. (E) An analysis of mRNA expression showed that CAP increased the levels of PGC-1α, Nrf-1, and TFAM. (F) Western blot analysis confirmed the upregulated expression of PGC-1α, Nrf-1, and TFAM proteins in LPS-stimulated HGF-1 cells following CAP treatment. Values are shown as mean ± SD, and statistical significance was considered at * p < 0.05, ** p < 0.01, and *** p < 0.001 when compared with the control group.
    Figure Legend Snippet: Cold atmospheric plasma (CAP) restores mitochondrial function in LPS-stimulated HGF-1 cells. (A) CAP maintained mitochondrial membrane potential, evaluated via TMRM staining, in inflammatory conditions. 200× magnification. The scale bar is 50 μm. (B) CAP reduced mitochondrial ROS (mtROS) levels, as evidenced by MitoSOX Red fluorescence. The original magnification was 200×, and the scale bar was 50 μm. (C) Quantification of ATP production showed that CAP treatment (30 s) markedly increased cellular ATP levels compared with the LPS-only group and even exceeded those of the untreated control. (D) Immunofluorescence staining of HSP60 showed that the shape and content of mitochondria improved after CAP exposure. (E) An analysis of mRNA expression showed that CAP increased the levels of PGC-1α, Nrf-1, and TFAM. (F) Western blot analysis confirmed the upregulated expression of PGC-1α, Nrf-1, and TFAM proteins in LPS-stimulated HGF-1 cells following CAP treatment. Values are shown as mean ± SD, and statistical significance was considered at * p < 0.05, ** p < 0.01, and *** p < 0.001 when compared with the control group.

    Techniques Used: Clinical Proteomics, Membrane, Staining, Fluorescence, Control, Immunofluorescence, Expressing, Western Blot

    CAP modulates the inflammatory response and mitochondrial function in a manner dependent on H 2 O 2 . (A) The relative expression levels of NF-κB, IL-6, IL-1β, and TNF-α mRNA in HGF-1 cells stimulated with LPS. CAP treatment (30 s) significantly diminished pro-inflammatory transcripts, whereas catalase (50 U/mL, H 2 O 2 scavenger) counteracted this effect. (B) Western blot analysis showing that CAP inhibits NF-κB and p-NF-κB. Catalase removed this suppression, which showed that it depended on H 2 O 2 . (C) ELISA quantification of TNF-α, IL-1β, and IL-6 protein concentrations. Catalase counteracted the substantial reduction in cytokine secretion induced by CAP. (D) TMRM staining showing that CAP preserved mitochondrial membrane potential in the presence of LPS, whereas catalase prevented this protective effect. (E) Measurement of ATP levels showed that CAP restored ATP production suppressed by LPS, whereas catalase abolished this recovery. (F) Western blot analysis of PGC-1α, Nrf-1, and TFAM showed that CAP increased markers of mitochondrial biogenesis, but catalase reversed this effect. All data are shown as mean ± SD, and statistical significance was defined as * p < 0.05, ** p < 0.01, and *** p < 0.001 when compared with the control group.
    Figure Legend Snippet: CAP modulates the inflammatory response and mitochondrial function in a manner dependent on H 2 O 2 . (A) The relative expression levels of NF-κB, IL-6, IL-1β, and TNF-α mRNA in HGF-1 cells stimulated with LPS. CAP treatment (30 s) significantly diminished pro-inflammatory transcripts, whereas catalase (50 U/mL, H 2 O 2 scavenger) counteracted this effect. (B) Western blot analysis showing that CAP inhibits NF-κB and p-NF-κB. Catalase removed this suppression, which showed that it depended on H 2 O 2 . (C) ELISA quantification of TNF-α, IL-1β, and IL-6 protein concentrations. Catalase counteracted the substantial reduction in cytokine secretion induced by CAP. (D) TMRM staining showing that CAP preserved mitochondrial membrane potential in the presence of LPS, whereas catalase prevented this protective effect. (E) Measurement of ATP levels showed that CAP restored ATP production suppressed by LPS, whereas catalase abolished this recovery. (F) Western blot analysis of PGC-1α, Nrf-1, and TFAM showed that CAP increased markers of mitochondrial biogenesis, but catalase reversed this effect. All data are shown as mean ± SD, and statistical significance was defined as * p < 0.05, ** p < 0.01, and *** p < 0.001 when compared with the control group.

    Techniques Used: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Staining, Membrane, Control



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    Image Search Results


    Cytotoxicity of CAP treatment in HGF-1 cells. Cell viability was assessed after CAP exposure at 6 and 24 h using the WST-8 assay. (A) 25–25 condition, (B) 50–50 condition, and (C) 75–75 condition. CAP treatment up to 180 s maintained cell viability above ∼ 80%, with slight reductions observed at longer exposure times under higher power conditions. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, compared to the control of 6 h. # p < 0.05, ## p < 0.01, compared to the control of 24 h.

    Journal: ACS Omega

    Article Title: Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation

    doi: 10.1021/acsomega.5c11346

    Figure Lengend Snippet: Cytotoxicity of CAP treatment in HGF-1 cells. Cell viability was assessed after CAP exposure at 6 and 24 h using the WST-8 assay. (A) 25–25 condition, (B) 50–50 condition, and (C) 75–75 condition. CAP treatment up to 180 s maintained cell viability above ∼ 80%, with slight reductions observed at longer exposure times under higher power conditions. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, compared to the control of 6 h. # p < 0.05, ## p < 0.01, compared to the control of 24 h.

    Article Snippet: Human gingival fibroblast (HGF-1) was purchased from American Type Culture Collection (Manassas, Virginia, USA).

    Techniques: Control

    CAP-induced production of RONS in HGF-1 cells. (A–C) Extracellular levels of nitric oxide (NO), hydroxyl radicals ( • OH), and singlet oxygen ( 1 O 2 ) increased in a time- and power-dependent manner following CAP treatment (25–25, 50–50, and 75–75 conditions). (D) Intracellular ROS accumulation was measured by fluorescence microscopy at 6 and 24 h. (E) H 2 O 2 concentrations were significantly elevated in a time-dependent manner, and (F) CAP increased intracellular NO levels. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001 versus control.

    Journal: ACS Omega

    Article Title: Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation

    doi: 10.1021/acsomega.5c11346

    Figure Lengend Snippet: CAP-induced production of RONS in HGF-1 cells. (A–C) Extracellular levels of nitric oxide (NO), hydroxyl radicals ( • OH), and singlet oxygen ( 1 O 2 ) increased in a time- and power-dependent manner following CAP treatment (25–25, 50–50, and 75–75 conditions). (D) Intracellular ROS accumulation was measured by fluorescence microscopy at 6 and 24 h. (E) H 2 O 2 concentrations were significantly elevated in a time-dependent manner, and (F) CAP increased intracellular NO levels. Data are expressed as mean ± SD, * p < 0.05, ** p < 0.01, *** p < 0.001 versus control.

    Article Snippet: Human gingival fibroblast (HGF-1) was purchased from American Type Culture Collection (Manassas, Virginia, USA).

    Techniques: Fluorescence, Microscopy, Control

    Effects of 30 s CAP exposure on NF-κB, inflammatory cytokines, and COL1A1 expression in HGF-1 cells under various plasma discharge conditions. The mRNA expression levels of (A) NF-κB, (B) IL-6, (C) IL-1β, (D) TNF-α, and (E) COL1A1 were evaluated at 6 and 24 h after treatment. The data are shown as fold change relative to the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: ACS Omega

    Article Title: Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation

    doi: 10.1021/acsomega.5c11346

    Figure Lengend Snippet: Effects of 30 s CAP exposure on NF-κB, inflammatory cytokines, and COL1A1 expression in HGF-1 cells under various plasma discharge conditions. The mRNA expression levels of (A) NF-κB, (B) IL-6, (C) IL-1β, (D) TNF-α, and (E) COL1A1 were evaluated at 6 and 24 h after treatment. The data are shown as fold change relative to the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Human gingival fibroblast (HGF-1) was purchased from American Type Culture Collection (Manassas, Virginia, USA).

    Techniques: Expressing, Clinical Proteomics, Control

    CAP inhibits NF-κB signaling and the expression of pro-inflammatory cytokines in LPS-stimulated HGF-1 cells. (A) qRT-PCR results showing the relative mRNA expression levels of NF-κB, IL-6, IL-1β, and TNF-α in LPS-stimulated cells treated with CAP (30 or 60 s) or NAC. (B) Western blot analysis of NF-κB and phosphorylated NF-κB (p-NF-κB) demonstrating CAP’s suppression of NF-κB activation. (C) ELISA measurement of the amounts of IL-6, IL-1β, and TNF-α proteins in the culture supernatants. The data are shown as fold change compared with the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: ACS Omega

    Article Title: Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation

    doi: 10.1021/acsomega.5c11346

    Figure Lengend Snippet: CAP inhibits NF-κB signaling and the expression of pro-inflammatory cytokines in LPS-stimulated HGF-1 cells. (A) qRT-PCR results showing the relative mRNA expression levels of NF-κB, IL-6, IL-1β, and TNF-α in LPS-stimulated cells treated with CAP (30 or 60 s) or NAC. (B) Western blot analysis of NF-κB and phosphorylated NF-κB (p-NF-κB) demonstrating CAP’s suppression of NF-κB activation. (C) ELISA measurement of the amounts of IL-6, IL-1β, and TNF-α proteins in the culture supernatants. The data are shown as fold change compared with the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Human gingival fibroblast (HGF-1) was purchased from American Type Culture Collection (Manassas, Virginia, USA).

    Techniques: Expressing, Quantitative RT-PCR, Western Blot, Activation Assay, Enzyme-linked Immunosorbent Assay, Control

    CAP enhances the regenerative response of LPS-stimulated HGF-1 cells. (A) Exposure to CAP for 30 s promoted cell migration under LPS-induced inflammatory conditions. (B) Immunofluorescence staining of COL1A1 (green) revealed that CAP treatment stimulated collagen synthesis, while nuclei were counterstained with DAPI (blue). (C) Cell viability assays performed at 12 and 24 h post-treatment showed that CAP promoted HGF-1 cell proliferation under inflammatory conditions. The data are shown as fold change compared with the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: ACS Omega

    Article Title: Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation

    doi: 10.1021/acsomega.5c11346

    Figure Lengend Snippet: CAP enhances the regenerative response of LPS-stimulated HGF-1 cells. (A) Exposure to CAP for 30 s promoted cell migration under LPS-induced inflammatory conditions. (B) Immunofluorescence staining of COL1A1 (green) revealed that CAP treatment stimulated collagen synthesis, while nuclei were counterstained with DAPI (blue). (C) Cell viability assays performed at 12 and 24 h post-treatment showed that CAP promoted HGF-1 cell proliferation under inflammatory conditions. The data are shown as fold change compared with the control (mean ± SD). * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: Human gingival fibroblast (HGF-1) was purchased from American Type Culture Collection (Manassas, Virginia, USA).

    Techniques: Migration, Immunofluorescence, Staining, Control

    Cold atmospheric plasma (CAP) restores mitochondrial function in LPS-stimulated HGF-1 cells. (A) CAP maintained mitochondrial membrane potential, evaluated via TMRM staining, in inflammatory conditions. 200× magnification. The scale bar is 50 μm. (B) CAP reduced mitochondrial ROS (mtROS) levels, as evidenced by MitoSOX Red fluorescence. The original magnification was 200×, and the scale bar was 50 μm. (C) Quantification of ATP production showed that CAP treatment (30 s) markedly increased cellular ATP levels compared with the LPS-only group and even exceeded those of the untreated control. (D) Immunofluorescence staining of HSP60 showed that the shape and content of mitochondria improved after CAP exposure. (E) An analysis of mRNA expression showed that CAP increased the levels of PGC-1α, Nrf-1, and TFAM. (F) Western blot analysis confirmed the upregulated expression of PGC-1α, Nrf-1, and TFAM proteins in LPS-stimulated HGF-1 cells following CAP treatment. Values are shown as mean ± SD, and statistical significance was considered at * p < 0.05, ** p < 0.01, and *** p < 0.001 when compared with the control group.

    Journal: ACS Omega

    Article Title: Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation

    doi: 10.1021/acsomega.5c11346

    Figure Lengend Snippet: Cold atmospheric plasma (CAP) restores mitochondrial function in LPS-stimulated HGF-1 cells. (A) CAP maintained mitochondrial membrane potential, evaluated via TMRM staining, in inflammatory conditions. 200× magnification. The scale bar is 50 μm. (B) CAP reduced mitochondrial ROS (mtROS) levels, as evidenced by MitoSOX Red fluorescence. The original magnification was 200×, and the scale bar was 50 μm. (C) Quantification of ATP production showed that CAP treatment (30 s) markedly increased cellular ATP levels compared with the LPS-only group and even exceeded those of the untreated control. (D) Immunofluorescence staining of HSP60 showed that the shape and content of mitochondria improved after CAP exposure. (E) An analysis of mRNA expression showed that CAP increased the levels of PGC-1α, Nrf-1, and TFAM. (F) Western blot analysis confirmed the upregulated expression of PGC-1α, Nrf-1, and TFAM proteins in LPS-stimulated HGF-1 cells following CAP treatment. Values are shown as mean ± SD, and statistical significance was considered at * p < 0.05, ** p < 0.01, and *** p < 0.001 when compared with the control group.

    Article Snippet: Human gingival fibroblast (HGF-1) was purchased from American Type Culture Collection (Manassas, Virginia, USA).

    Techniques: Clinical Proteomics, Membrane, Staining, Fluorescence, Control, Immunofluorescence, Expressing, Western Blot

    CAP modulates the inflammatory response and mitochondrial function in a manner dependent on H 2 O 2 . (A) The relative expression levels of NF-κB, IL-6, IL-1β, and TNF-α mRNA in HGF-1 cells stimulated with LPS. CAP treatment (30 s) significantly diminished pro-inflammatory transcripts, whereas catalase (50 U/mL, H 2 O 2 scavenger) counteracted this effect. (B) Western blot analysis showing that CAP inhibits NF-κB and p-NF-κB. Catalase removed this suppression, which showed that it depended on H 2 O 2 . (C) ELISA quantification of TNF-α, IL-1β, and IL-6 protein concentrations. Catalase counteracted the substantial reduction in cytokine secretion induced by CAP. (D) TMRM staining showing that CAP preserved mitochondrial membrane potential in the presence of LPS, whereas catalase prevented this protective effect. (E) Measurement of ATP levels showed that CAP restored ATP production suppressed by LPS, whereas catalase abolished this recovery. (F) Western blot analysis of PGC-1α, Nrf-1, and TFAM showed that CAP increased markers of mitochondrial biogenesis, but catalase reversed this effect. All data are shown as mean ± SD, and statistical significance was defined as * p < 0.05, ** p < 0.01, and *** p < 0.001 when compared with the control group.

    Journal: ACS Omega

    Article Title: Cold Atmospheric Plasma Promotes Anti-Inflammatory and Regenerative Responses in Oral Soft Tissue through Redox-Driven Mitochondrial Regulation

    doi: 10.1021/acsomega.5c11346

    Figure Lengend Snippet: CAP modulates the inflammatory response and mitochondrial function in a manner dependent on H 2 O 2 . (A) The relative expression levels of NF-κB, IL-6, IL-1β, and TNF-α mRNA in HGF-1 cells stimulated with LPS. CAP treatment (30 s) significantly diminished pro-inflammatory transcripts, whereas catalase (50 U/mL, H 2 O 2 scavenger) counteracted this effect. (B) Western blot analysis showing that CAP inhibits NF-κB and p-NF-κB. Catalase removed this suppression, which showed that it depended on H 2 O 2 . (C) ELISA quantification of TNF-α, IL-1β, and IL-6 protein concentrations. Catalase counteracted the substantial reduction in cytokine secretion induced by CAP. (D) TMRM staining showing that CAP preserved mitochondrial membrane potential in the presence of LPS, whereas catalase prevented this protective effect. (E) Measurement of ATP levels showed that CAP restored ATP production suppressed by LPS, whereas catalase abolished this recovery. (F) Western blot analysis of PGC-1α, Nrf-1, and TFAM showed that CAP increased markers of mitochondrial biogenesis, but catalase reversed this effect. All data are shown as mean ± SD, and statistical significance was defined as * p < 0.05, ** p < 0.01, and *** p < 0.001 when compared with the control group.

    Article Snippet: Human gingival fibroblast (HGF-1) was purchased from American Type Culture Collection (Manassas, Virginia, USA).

    Techniques: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay, Staining, Membrane, Control

    PM induces COX-2-dependent PGE 2 and MMP-1 production. (A and B) HGF-1 cells were treated with different concentrations of PM for 24 h, or with 50 μg/cm 2 of PM for various time points, and cell viability was then measured. HGF-1 cells were treated with 50 μg/cm 2 of PM for different time points, and (C) COX-2 protein levels, (D) PGE 2 release, (E) MMP-1 mRNA expression, and (F) MMP-1 release were measured. (G) HGF-1 cells were pretreated with NS-398 and then exposed to PM, after which MMP-1 mRNA expression and release were examined. Data are presented as mean ± SD from at least three independent experiments. ∗ P < 0.05, # P < 0.01 compared with the control group (A, C–F). # P < 0.01 compared with cells exposed to PM alone. PM: particulate matter; COX-2: cyclooxygenase-2; PGE 2 : prostaglandin E 2 ; MMP-1: matrix metalloproteinase-1; HGF-1: human gingival fibroblast.

    Journal: Journal of Dental Sciences

    Article Title: Nuclear factor erythroid 2-related factor 2/heme oxygenase-1 activation by nattokinase reduces pro-inflammatory and matrix-degrading mediators in human gingival fibroblasts

    doi: 10.1016/j.jds.2025.10.022

    Figure Lengend Snippet: PM induces COX-2-dependent PGE 2 and MMP-1 production. (A and B) HGF-1 cells were treated with different concentrations of PM for 24 h, or with 50 μg/cm 2 of PM for various time points, and cell viability was then measured. HGF-1 cells were treated with 50 μg/cm 2 of PM for different time points, and (C) COX-2 protein levels, (D) PGE 2 release, (E) MMP-1 mRNA expression, and (F) MMP-1 release were measured. (G) HGF-1 cells were pretreated with NS-398 and then exposed to PM, after which MMP-1 mRNA expression and release were examined. Data are presented as mean ± SD from at least three independent experiments. ∗ P < 0.05, # P < 0.01 compared with the control group (A, C–F). # P < 0.01 compared with cells exposed to PM alone. PM: particulate matter; COX-2: cyclooxygenase-2; PGE 2 : prostaglandin E 2 ; MMP-1: matrix metalloproteinase-1; HGF-1: human gingival fibroblast.

    Article Snippet: Human gingival fibroblasts (HGF-1, ATCC CRL-2014; Manassas, VA, USA) were cultured in Dulbecco's Modified Eagle's Medium (DMEM, ATCC 30–2002) supplemented with 10 % fetal bovine serum (FBS), 100 μg/ml streptomycin, and 100 U/ml penicillin, at 37 °C in a humidified 5 % CO 2 atmosphere.

    Techniques: Expressing, Control

    Intrinsic cytotoxicity of CPX or HAgCPX nanoparticles. ( A ) HGF-1 cells; ( B ) L929 cells. CPX or HAgCPX nanoparticles in serum free media were treated to cells for 1 day. CPX in DMSO was diluted more than 100 times with cell culture media and then treated to cells. HAgCPX nanoparticles and/or free HA in aqueous solution were sterilized with a 1.2 µm syringe filter and then diluted cell culture media following treatment against cells. The significance is as follows: ns; not significant.

    Journal: Scientific Reports

    Article Title: Reactive oxygen species-sensitive release of cephalexin from hyaluronic acid- g -cephalexin dimer copolymer for treatment of inflammation and infection of oral soft tissue cells

    doi: 10.1038/s41598-025-30912-7

    Figure Lengend Snippet: Intrinsic cytotoxicity of CPX or HAgCPX nanoparticles. ( A ) HGF-1 cells; ( B ) L929 cells. CPX or HAgCPX nanoparticles in serum free media were treated to cells for 1 day. CPX in DMSO was diluted more than 100 times with cell culture media and then treated to cells. HAgCPX nanoparticles and/or free HA in aqueous solution were sterilized with a 1.2 µm syringe filter and then diluted cell culture media following treatment against cells. The significance is as follows: ns; not significant.

    Article Snippet: Human gingival fibroblast-1 (HGF-1) cells were purchased from American Type Culture Collection (ATCC, Manassas, Virginia, USA).

    Techniques: Cell Culture

    Anti-inflammatory effect of CPX or HAgCPX nanoparticles against LPS-treated HGF-1 cells. ( A ) Cell viability; ( B ) Expression of inflammatory cytokines such as IL-6 and TNF-α. For evaluation of inflammatory cytokines, CPX or HAgCPX nanoparticles were treated to cells. Final concentration was 20 µg/mL based on CPX) were treated to cells. HAgCPX nanoparticles in aqueous solution were diluted with media to be 20 µg CPX/mL. ( C ) Wound healing assay. Cells were treated with CPX or HAgCPX nanoparticles for 12 h. The dose of drug was 20 µg/mL based on CPX both of CPX or HAgCPX nanoparticles. After that, LPS (10 μg/ml) was treated to cells for 12 h. Cells were scratched and the cells were cultured for 48 h. The significance is as follows: #### p < 0.0001 compared with the control group; ** p < 0.01, *** p < 0.001, **** p < 0.0001 compared with the LPS control group; n., not significant.

    Journal: Scientific Reports

    Article Title: Reactive oxygen species-sensitive release of cephalexin from hyaluronic acid- g -cephalexin dimer copolymer for treatment of inflammation and infection of oral soft tissue cells

    doi: 10.1038/s41598-025-30912-7

    Figure Lengend Snippet: Anti-inflammatory effect of CPX or HAgCPX nanoparticles against LPS-treated HGF-1 cells. ( A ) Cell viability; ( B ) Expression of inflammatory cytokines such as IL-6 and TNF-α. For evaluation of inflammatory cytokines, CPX or HAgCPX nanoparticles were treated to cells. Final concentration was 20 µg/mL based on CPX) were treated to cells. HAgCPX nanoparticles in aqueous solution were diluted with media to be 20 µg CPX/mL. ( C ) Wound healing assay. Cells were treated with CPX or HAgCPX nanoparticles for 12 h. The dose of drug was 20 µg/mL based on CPX both of CPX or HAgCPX nanoparticles. After that, LPS (10 μg/ml) was treated to cells for 12 h. Cells were scratched and the cells were cultured for 48 h. The significance is as follows: #### p < 0.0001 compared with the control group; ** p < 0.01, *** p < 0.001, **** p < 0.0001 compared with the LPS control group; n., not significant.

    Article Snippet: Human gingival fibroblast-1 (HGF-1) cells were purchased from American Type Culture Collection (ATCC, Manassas, Virginia, USA).

    Techniques: Expressing, Concentration Assay, Wound Healing Assay, Cell Culture, Control

    Apoptosis/necrosis analysis of HGF-1 cells. Cells were treated with CPX or HAgCPX nanoparticles. The dose of drug was 20 µg/ml based on CPX. HAgCPX nanoparticles in aqueous solution were diluted with media to be 20 µg CPX/mL. These were washed with PBS once more and then LPS (10 μg/ml) was treated to cells for 12 h. FITC–annexin V (FITC-A) and propidium iodide (PI) were used to analyze apoptosis and necrosis, respectively.

    Journal: Scientific Reports

    Article Title: Reactive oxygen species-sensitive release of cephalexin from hyaluronic acid- g -cephalexin dimer copolymer for treatment of inflammation and infection of oral soft tissue cells

    doi: 10.1038/s41598-025-30912-7

    Figure Lengend Snippet: Apoptosis/necrosis analysis of HGF-1 cells. Cells were treated with CPX or HAgCPX nanoparticles. The dose of drug was 20 µg/ml based on CPX. HAgCPX nanoparticles in aqueous solution were diluted with media to be 20 µg CPX/mL. These were washed with PBS once more and then LPS (10 μg/ml) was treated to cells for 12 h. FITC–annexin V (FITC-A) and propidium iodide (PI) were used to analyze apoptosis and necrosis, respectively.

    Article Snippet: Human gingival fibroblast-1 (HGF-1) cells were purchased from American Type Culture Collection (ATCC, Manassas, Virginia, USA).

    Techniques:

    Effect of LPS on the expression of CD44 receptor in the HGF-1 cells. ( A ) Expression of CD44 receptor in HGF-1 cells: (a) Fluorescence microscopy and (b) Flow cytometry. ( B ) CD44 receptor interaction of rhodamine B-labelled HAgCPX nanoparticles (HAgCPX NP) with LPS-treated HGF-1 cells: (a) Fluorescence microscopy; (b) flowcytometry. Free HA (0 mg/ml, 1 mg/ml or 10 mg/ml) was added to cell culture to block CD44 receptor of LPS-treated HGF-1 cells. The dose of drug was 20 µg/ml based on CPX. HAgCPX nanoparticles in aqueous solution were diluted with media to be 20 µg CPX/mL. One h later, cells were treated with rhodamine B-labelled HAgCPX nanoparticles for 90 min. Bar = 100 μm.

    Journal: Scientific Reports

    Article Title: Reactive oxygen species-sensitive release of cephalexin from hyaluronic acid- g -cephalexin dimer copolymer for treatment of inflammation and infection of oral soft tissue cells

    doi: 10.1038/s41598-025-30912-7

    Figure Lengend Snippet: Effect of LPS on the expression of CD44 receptor in the HGF-1 cells. ( A ) Expression of CD44 receptor in HGF-1 cells: (a) Fluorescence microscopy and (b) Flow cytometry. ( B ) CD44 receptor interaction of rhodamine B-labelled HAgCPX nanoparticles (HAgCPX NP) with LPS-treated HGF-1 cells: (a) Fluorescence microscopy; (b) flowcytometry. Free HA (0 mg/ml, 1 mg/ml or 10 mg/ml) was added to cell culture to block CD44 receptor of LPS-treated HGF-1 cells. The dose of drug was 20 µg/ml based on CPX. HAgCPX nanoparticles in aqueous solution were diluted with media to be 20 µg CPX/mL. One h later, cells were treated with rhodamine B-labelled HAgCPX nanoparticles for 90 min. Bar = 100 μm.

    Article Snippet: Human gingival fibroblast-1 (HGF-1) cells were purchased from American Type Culture Collection (ATCC, Manassas, Virginia, USA).

    Techniques: Expressing, Fluorescence, Microscopy, Flow Cytometry, Cell Culture, Blocking Assay

    Effect of pre-treatment of free HA on the secretion of cytokine. Secretion of inflammatory cytokines such as IL-6 ( A ) and TNF-α ( B ). CD44 receptor of HGF-1 cells was blocked with pre-treatment of free HA (final concentration, 1 mg/mL) for competition assay. For evaluation of inflammatory cytokines, CPX or HAgCPX nanoparticles were treated to cells. Final concentration was 20 µg/mL based on CPX) were treated to cells. HAgCPX nanoparticles in aqueous solution were diluted with media to be 20 µg CPX/mL. The significance is as follows: #### p < 0.0001 compared with the control group; **** p < 0.0001 compared with the LPS group; ns, not significant.

    Journal: Scientific Reports

    Article Title: Reactive oxygen species-sensitive release of cephalexin from hyaluronic acid- g -cephalexin dimer copolymer for treatment of inflammation and infection of oral soft tissue cells

    doi: 10.1038/s41598-025-30912-7

    Figure Lengend Snippet: Effect of pre-treatment of free HA on the secretion of cytokine. Secretion of inflammatory cytokines such as IL-6 ( A ) and TNF-α ( B ). CD44 receptor of HGF-1 cells was blocked with pre-treatment of free HA (final concentration, 1 mg/mL) for competition assay. For evaluation of inflammatory cytokines, CPX or HAgCPX nanoparticles were treated to cells. Final concentration was 20 µg/mL based on CPX) were treated to cells. HAgCPX nanoparticles in aqueous solution were diluted with media to be 20 µg CPX/mL. The significance is as follows: #### p < 0.0001 compared with the control group; **** p < 0.0001 compared with the LPS group; ns, not significant.

    Article Snippet: Human gingival fibroblast-1 (HGF-1) cells were purchased from American Type Culture Collection (ATCC, Manassas, Virginia, USA).

    Techniques: Concentration Assay, Competitive Binding Assay, Control